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1. Haas SL, Jesnowski R, Steiner M, Hummel F, Ringel J, Burstein C, Nizze H, Liebe S, Löhr JM: Expression of tissue factor in pancreatic adenocarcinoma is associated with activation of coagulation. World J Gastroenterol; 2006 Aug 14;12(30):4843-9
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  • [Title] Expression of tissue factor in pancreatic adenocarcinoma is associated with activation of coagulation.
  • AIM: To study expression of tissue factor (TF) in pancreatic cancer and its role in the development of thromboembolism.
  • METHODS: TF expression was studied in eight human pancreatic carcinoma cell lines by Northern blot and indirect immunofluorescence.
  • In addition, TF expression was determined by immunofluorescence in pancreatic tissues of 19 patients with pancreatic adenocarcinoma (PCa), 9 patients with chronic pancreatitis (CP) and 20 normal controls.
  • RESULTS: All pancreatic carcinoma cell lines expressed TF (8/8) and most of them expressed asTF (6/8).
  • TF expression at the protein level did not correlate with the differentiation of the carcinoma cell line.
  • All but two pancreatic cancer tissue samples stained positive for TF (17/19).
  • In all samples of CP weak staining was restricted to pancreatic duct cells, whereas only a few subendothelial cells were positive in 9/20 of normal controls.
  • CONCLUSION: We conclude that in addition to the upregulated expression of TF on the cell membrane, soluble TF might contribute to activation of the coagulation system in pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Blood Coagulation. Pancreatic Neoplasms / metabolism. Thromboembolism / metabolism. Thromboplastin / metabolism
  • [MeSH-minor] Aged. Cell Line, Tumor. Female. Humans. Male. Middle Aged

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  • [Cites] Nat Med. 2003 Apr;9(4):458-62 [12652293.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4461-7 [9766679.001]
  • [Cites] Virchows Arch. 2003 May;442(5):444-52 [12692724.001]
  • [Cites] Eur J Surg Oncol. 2003 Jun;29(5):417-22 [12798743.001]
  • [Cites] Chest. 2003 Sep;124(3 Suppl):58S-68S [12970125.001]
  • [Cites] Crit Care Med. 2004 May;32(5 Suppl):S293-7 [15118533.001]
  • [Cites] Nat Med. 2004 May;10(5):502-9 [15098027.001]
  • [Cites] Thromb Haemost. 2004 Jul;92(1):132-9 [15213854.001]
  • [Cites] Br J Cancer. 2004 Jul 5;91(1):92-5 [15226761.001]
  • [Cites] J Biol Chem. 2004 Aug 20;279(34):36142-7 [15201277.001]
  • [Cites] Histopathology. 1985 Aug;9(8):841-56 [2997015.001]
  • [Cites] N Engl J Med. 1986 Dec 25;315(26):1650-9 [3537791.001]
  • [Cites] Br J Cancer. 1999 Feb;79(3-4):472-7 [10027315.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2311-5 [10051638.001]
  • [Cites] Atherosclerosis. 1999 Jun;144(2):273-83 [10407489.001]
  • [Cites] Medicine (Baltimore). 1999 Sep;78(5):285-91 [10499070.001]
  • [Cites] J Thromb Haemost. 2004 Nov;2(11):2065-7 [15550054.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2005 Jan;25(1):47-56 [15569823.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1734-41 [15494427.001]
  • [Cites] Neoplasia. 2005 Jan;7(1):17-23 [15720814.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1406-13 [15735028.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2531-9 [15814630.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1604-11 [15741221.001]
  • [Cites] Cell. 1987 Jul 3;50(1):129-35 [3297348.001]
  • [Cites] Am J Pathol. 1989 May;134(5):1087-97 [2719077.001]
  • [Cites] Thromb Res. 1990 Jul 15;59(2):421-37 [2237820.001]
  • [Cites] J Biol Chem. 1991 Aug 25;266(24):15719-25 [1874730.001]
  • [Cites] N Engl J Med. 1992 May 7;326(19):1240-5 [1560799.001]
  • [Cites] J Neurosci. 1992 Dec;12(12):4905-10 [1281498.001]
  • [Cites] Pancreas. 1993 Mar;8(2):248-54 [8460098.001]
  • [Cites] Br J Cancer. 1994 Jan;69(1):144-51 [8286197.001]
  • [Cites] J Clin Invest. 1994 Sep;94(3):1320-7 [7521887.001]
  • [Cites] J Biol Chem. 1995 Feb 24;270(8):3849-57 [7876129.001]
  • [Cites] FASEB J. 1995 Jul;9(10):883-9 [7615158.001]
  • [Cites] Br J Surg. 1995 Aug;82(8):1101-4 [7648165.001]
  • [Cites] J Biol Chem. 1995 Nov 3;270(44):26419-32 [7592857.001]
  • [Cites] Nat Med. 1996 Feb;2(2):209-15 [8574967.001]
  • [Cites] Gastroenterology. 2000 Feb;118(2):356-67 [10648464.001]
  • [Cites] Arch Intern Med. 2000 Mar 27;160(6):809-15 [10737280.001]
  • [Cites] Lancet. 2000 May 6;355(9215):1627-32 [10821379.001]
  • [Cites] Br J Cancer. 2000 Jul;83(2):164-70 [10901365.001]
  • [Cites] N Engl J Med. 2000 Dec 21;343(25):1846-50 [11117976.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):550-5 [11212248.001]
  • [Cites] Circulation. 2001 Jun 26;103(25):3044-6 [11425765.001]
  • [Cites] J Gastroenterol. 2001 Dec;36(12):848-50 [11777214.001]
  • [Cites] Biochem Soc Trans. 2002 Apr;30(2):173-7 [12023846.001]
  • [Cites] Clin Biochem. 2002 Jun;35(4):321-5 [12135696.001]
  • [Cites] Curr Opin Hematol. 2002 Sep;9(5):401-6 [12172458.001]
  • [Cites] Ann Intern Med. 1996 Jul 1;125(1):1-7 [8644983.001]
  • [Cites] Pancreas. 1996 Apr;12(3):248-59 [8830331.001]
  • [Cites] Thromb Haemost. 1997 Jul;78(1):121-5 [9198140.001]
  • [Cites] Int J Cancer. 1998 Feb 20;79(1):19-22 [9495352.001]
  • [Cites] Pancreas. 1998 Mar;16(2):189-94 [9510143.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4216-23 [9596669.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4387-92 [12560220.001]
  • (PMID = 16937466.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 9035-58-9 / Thromboplastin
  • [Other-IDs] NLM/ PMC4087618
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2. Al-Wadei HA, Majidi M, Tsao MS, Schuller HM: Low concentrations of beta-carotene stimulate the proliferation of human pancreatic duct epithelial cells in a PKA-dependent manner. Cancer Genomics Proteomics; 2007 Jan-Feb;4(1):35-42
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  • [Title] Low concentrations of beta-carotene stimulate the proliferation of human pancreatic duct epithelial cells in a PKA-dependent manner.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is among the most common causes of cancer death.
  • While some of the preclinical data suggested cancer preventive effects of these agents, they have disappointed in clinical investigations.
  • MATERIALS AND METHODS: The effects of low concentrations (10 fM-200 nM)of beta-carotene on the proliferation, intracellular cAMP levels, PKA activation status and phosphorylation of EGFR-specific tyrosine kinases and ERK1/2 in immortalized human pancreatic duct epithelial cells was investigated.
  • Our data indicate that low concentrations of beta-carotene stimulate the proliferation of the putative origin of PDAC, pancreatic duct epithelial cells via cAMP and PKA-dependent transactivation of the EGFR pathway.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinases / metabolism. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Pancreatic Ducts / cytology. Pancreatic Ducts / drug effects. beta Carotene / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Colforsin / pharmacology. Enzyme Activation / drug effects. Enzyme Induction / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / biosynthesis. Mitogen-Activated Protein Kinase 3 / biosynthesis. Phosphorylation / drug effects. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 17726239.001).
  • [ISSN] 1109-6535
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA42829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 01YAE03M7J / beta Carotene; 1F7A44V6OU / Colforsin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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3. Hashimoto Y, Murakami Y, Uemura K, Hayashidani Y, Sudo T, Ohge H, Fukuda E, Sueda T, Hiyama E: Detection of human telomerase reverse transcriptase (hTERT) expression in tissue and pancreatic juice from pancreatic cancer. Surgery; 2008 Jan;143(1):113-25
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  • [Title] Detection of human telomerase reverse transcriptase (hTERT) expression in tissue and pancreatic juice from pancreatic cancer.
  • BACKGROUND: Human telomerase reverse transcriptase (hTERT), a catalytic subunit of telomerase, is a promising diagnostic candidate for pancreatic cancer.
  • To evaluate the feasibility of immunohistochemistry (IHC) for the diagnosis of pancreatic cancer, hTERT expression and telomerase activity were assayed in pancreatic tissues, ex vivo brushing, and pancreatic juice samples with various pancreatic diseases.
  • METHODS: Telomerase activity was analyzed using the TRAP assay and hTERT was examined by IHC in 85 pancreatic tumor samples, 17 ex vivo pancreatic duct brushings, and 27 pancreatic juice samples.
  • In pancreatic juice samples, 10 of 11 IDCs and 3 of 4 malignant IPMNs expressed hTERT, in which seven samples were not diagnosed as malignant on cytologic exam.
  • The diagnoses of pancreatic cancer based on hTERT IHC exhibited high rates of sensitivity (87%), specificity (92%), and overall accuracy (89%), whereas the sensitivity of cytologic examination was 53%.
  • CONCLUSIONS: Our results suggested that hTERT expression in epithelia indicates malignant transformation in pancreatic tumors and immunohistochemical detection of hTERT in cells derived from pancreatic juice provides a potent method for cancer diagnosis.
  • [MeSH-major] Pancreatic Juice / chemistry. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / diagnosis. Telomerase / analysis
  • [MeSH-minor] Adenocarcinoma, Mucinous / chemistry. Adult. Aged. Aged, 80 and over. Carcinoma, Pancreatic Ductal / chemistry. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / chemistry. Cell Line, Tumor. Chronic Disease. Feasibility Studies. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Pancreatitis / metabolism. Sensitivity and Specificity

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  • (PMID = 18154939.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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4. Omura N, Li CP, Li A, Hong SM, Walter K, Jimeno A, Hidalgo M, Goggins M: Genome-wide profiling of methylated promoters in pancreatic adenocarcinoma. Cancer Biol Ther; 2008 Jul;7(7):1146-56
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  • [Title] Genome-wide profiling of methylated promoters in pancreatic adenocarcinoma.
  • RESULTS: 1,010 of 87,922 probes on the 88 K promoter array (606 genes) had a higher signal (log(2) > 2) in the pancreatic cancer line, Panc-1 compared to the non-neoplastic pancreatic duct line, HPDE.
  • More than 1/2 of the genes aberrantly hypermethylated in Panc-1 were not expressed in the pancreatic duct (HPDE) by expression array analysis.
  • Using the 244 K CpG island array, 1,968 CpG islands were differentially methylated in MiaPaca2 compared to normal pancreas.
  • Analysis of 57 pancreatic cancers and 34 normal pancreata using MSP identified MDFI, hsa-miR-9-1, ZNF415, CNTNAP2 and ELOVL4 as methylated in 96%, 89%, 86%, 82% and 68% of the cancers vs. 9%, 15%, 6%, 3% and 97% of normal pancreata, respectively.
  • METHODS: We used methylated CpG island amplification (MCA) and Agilent promoter and CpG island microarrays to identify differential DNA methylation patterns in pancreatic cancer vs. normal pancreas.
  • CONCLUSION: Promoter and CpG island array analysis finds aberrant methylation of hundreds of promoters and CpG islands in pancreatic cancer cells.

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  • [Cites] Cancer Res. 2001 Dec 1;61(23):8540-6 [11731440.001]
  • [Cites] PLoS Genet. 2007 Oct;3(10):2023-36 [17967063.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1573-81 [12000709.001]
  • [Cites] Nat Genet. 2002 Jun;31(2):141-9 [11992124.001]
  • [Cites] Gastroenterology. 2002 Jul;123(1):365-72 [12105864.001]
  • [Cites] Cancer Biol Ther. 2003 Jan-Feb;2(1):78-83 [12673124.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3735-42 [12839967.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4158-66 [12874021.001]
  • [Cites] Ann Hum Genet. 2003 May;67(Pt 3):242-9 [12914576.001]
  • [Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2307-12 [10344734.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8681-6 [10411935.001]
  • [Cites] Oncogene. 2005 Jan 27;24(5):850-8 [15592528.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):573-83 [15701843.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4681-8 [16000561.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-9 [16009939.001]
  • [Cites] Cell. 2005 Sep 23;122(6):947-56 [16153702.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Aug;3(8):752-60 [16234003.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):1208-17 [16424060.001]
  • [Cites] Nucleic Acids Res. 2006;34(2):528-42 [16428248.001]
  • [Cites] Nat Genet. 2006 Feb;38(2):149-53 [16444255.001]
  • [Cites] Gastroenterology. 2006 Feb;130(2):548-65 [16472607.001]
  • [Cites] Genome Res. 2006 Mar;16(3):383-93 [16449502.001]
  • [Cites] Science. 2002 Feb 8;295(5557):1079-82 [11834837.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2006;13(4):280-5 [16858538.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2006;13(4):286-95 [16858539.001]
  • [Cites] Mod Pathol. 2008 Mar;21(3):238-44 [18157091.001]
  • [Cites] Oncogene. 2008 Jun 5;27(25):3556-66 [18223687.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14440-4 [10588724.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):132-8 [10655057.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4652-61 [16899615.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7939-47 [16912168.001]
  • [Cites] Genes Dev. 2006 Dec 1;20(23):3215-31 [17158741.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):232-6 [17200670.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):237-42 [17211412.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2617-25 [17363581.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5527-32 [17369352.001]
  • [Cites] Genome Res. 2007 Oct;17(10):1529-36 [17785535.001]
  • [Cites] PLoS Genet. 2007 Sep;3(9):1709-23 [17892325.001]
  • [CommentIn] Cancer Biol Ther. 2008 Jul;7(7):1157-9 [18698160.001]
  • (PMID = 18535405.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA062924-090008; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA062924-130008; United States / NCI NIH HHS / CA / CA062924-110008; United States / NCI NIH HHS / CA / P50 CA062924-120008; United States / NCI NIH HHS / CA / P50 CA062924-100008; United States / NCI NIH HHS / CA / P50 CA062924-090008; United States / NCI NIH HHS / CA / CA062924-120008; United States / NCI NIH HHS / CA / P50 CA062924-130008; United States / NCI NIH HHS / CA / P50 CA062924-110008; United States / NCI NIH HHS / CA / CA062924-100008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS107839; NLM/ PMC2763640
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5. Lee KE, Bar-Sagi D: Oncogenic KRas suppresses inflammation-associated senescence of pancreatic ductal cells. Cancer Cell; 2010 Nov 16;18(5):448-58
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  • [Title] Oncogenic KRas suppresses inflammation-associated senescence of pancreatic ductal cells.
  • Mutational activation of KRas is the first and most frequently detected genetic lesion in pancreatic ductal adenocarcinoma (PDAC).
  • Here, we report that the endogenous expression of oncogenic KRas suppresses premature senescence in primary pancreatic duct epithelial cells (PDEC).
  • Moreover, the KRas-Twist-p16(INK4A) senescence bypass pathway is employed in vivo to prevent inflammation-associated senescence of pancreatic ductal epithelium.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):2969-72 [10955772.001]
  • [Cites] Dev Biol. 1995 Nov;172(1):280-92 [7589808.001]
  • [Cites] J Biol Chem. 2001 Jul 13;276(28):26699-707 [11323435.001]
  • [Cites] Nature. 2001 Sep 6;413(6851):86-91 [11544531.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):128-34 [12185368.001]
  • [Cites] Gut. 2002 Dec;51(6):849-52 [12427788.001]
  • [Cites] Nat Rev Cancer. 2003 Jan;3(1):11-22 [12509763.001]
  • [Cites] Cell. 2003 Jan 24;112(2):169-80 [12553906.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1906-13 [12702582.001]
  • [Cites] Cell. 1996 Apr 5;85(1):27-37 [8620534.001]
  • [Cites] Cell. 1997 Mar 7;88(5):593-602 [9054499.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2140-3 [9187111.001]
  • [Cites] Am J Physiol. 1997 Sep;273(3 Pt 1):G696-705 [9316474.001]
  • [Cites] Am J Surg. 1998 Jan;175(1):76-83 [9445247.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4740-4 [9788631.001]
  • [Cites] Gut. 1998 Sep;43(3):408-13 [9863488.001]
  • [Cites] J Clin Invest. 2004 Nov;114(9):1299-307 [15520862.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):307-15 [15549092.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):642 [16079833.001]
  • [Cites] Am J Physiol Cell Physiol. 2005 Nov;289(5):C1085-93 [16014704.001]
  • [Cites] Methods Enzymol. 2006;407:703-10 [16757363.001]
  • [Cites] Curr Biol. 2006 Nov 7;16(21):2173-9 [17084704.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Nat Cell Biol. 2007 May;9(5):493-505 [17450133.001]
  • [Cites] Mol Cell Biol. 2007 Jun;27(11):3920-35 [17403902.001]
  • [Cites] Cell. 2007 Jul 27;130(2):223-33 [17662938.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40 [17667954.001]
  • [Cites] Carcinogenesis. 2007 Dec;28(12):2467-75 [17690110.001]
  • [Cites] Am J Pathol. 2008 Apr;172(4):926-39 [18349132.001]
  • [Cites] Cell. 2008 Jun 13;133(6):1006-18 [18555777.001]
  • [Cites] Cell. 2008 Jun 13;133(6):1019-31 [18555778.001]
  • [Cites] Cancer Cell. 2008 Jul 8;14(1):79-89 [18598946.001]
  • [Cites] Nat Rev Cancer. 2009 Feb;9(2):81-94 [19132009.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2218-23 [19171888.001]
  • [Cites] J Exp Clin Cancer Res. 2009;28:28 [19243631.001]
  • [Cites] Biochem Biophys Res Commun. 2009 May 8;382(3):561-5 [19292977.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Gastroenterology. 2009 Sep;137(3):1072-82, 1082.e1-6 [19501586.001]
  • [Cites] Eur J Cancer. 2009 Sep;45 Suppl 1:211-6 [19775620.001]
  • [Cites] Cancer Cell. 2009 Nov 6;16(5):379-89 [19878870.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Nov 10;106(45):19035-9 [19858489.001]
  • [Cites] Annu Rev Pathol. 2010;5:99-118 [20078217.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):246-51 [20018721.001]
  • [Cites] J Clin Invest. 2010 Feb;120(2):508-20 [20071774.001]
  • [Cites] Cancer Cell. 2010 Aug 9;18(2):135-46 [20708155.001]
  • [Cites] J Clin Invest. 2004 Jan;113(1):8-13 [14702100.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Cancer Cell. 2004 Apr;5(4):375-87 [15093544.001]
  • [Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5659-63 [15313904.001]
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] N Engl J Med. 1992 Feb 13;326(7):455-65 [1732772.001]
  • [Cites] Eur Surg Res. 1992;24 Suppl 1:29-39 [1601022.001]
  • [Cites] N Engl J Med. 1993 May 20;328(20):1433-7 [8479461.001]
  • [Cites] Curr Biol. 1994 Jan 1;4(1):1-7 [7922305.001]
  • [Cites] Cell. 2000 Aug 18;102(4):407-10 [10966103.001]
  • (PMID = 21075310.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055360; United States / NCI NIH HHS / CA / R37 CA055360; United States / NCI NIH HHS / CA / R56 CA055360; United States / NCI NIH HHS / CA / CA055360
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; 0 / Twist Transcription Factor; 136253-27-5 / Twist1 protein, mouse; EC 3.2.1.23 / beta-Galactosidase; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS249223; NLM/ PMC3397918
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6. Sato M, Okumura T, Kaito K, Kiyoshima M, Asato Y, Uchiumi K, Iijima H, Hashimoto I, Kaburagi T, Amemiya R: Usefulness of FDG-PET/CT in the detection of pancreatic metastases from lung cancer. Ann Nucl Med; 2009 Jan;23(1):49-57
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  • [Title] Usefulness of FDG-PET/CT in the detection of pancreatic metastases from lung cancer.
  • OBJECTIVE: The objective of this study was to assess the ability to detect pancreatic metastasis of lung cancer and to clarify the degree of fluorodeoxyglucose (FDG) accumulation and computed tomography (CT) characteristics of pancreatic metastasis from lung cancer.
  • METHODS: A total of 573 patients (415 men and 158 women) with lung cancer were retrospectively evaluated.
  • RESULTS: Abnormal accumulations in the pancreas were detected in 5 of 313 patients (1.60%) in the initial study group, and 6 of 260 patients (2.31%) in the follow-up study group.
  • Seven of these patients had adenocarcinoma, three had small cell carcinoma, and the rest had large cell endocrine carcinoma.
  • Three of these pancreatic lesions were difficult to determine by routine transaxial images, and detection was obvious only by thin-slice images or multiplanar reconstruction images.
  • In addition, 10 of 11 cases did not show main pancreatic duct dilatation even if the tumor size was large.
  • CONCLUSIONS: Metastases to the pancreas in lung cancer patients are not so rare and radiologists first have an important role to detect the pancreatic mass and then suggest to metastasis as the likely diagnosis.
  • For this purpose, FDG-PET/CT has an advantage in depicting unsuspected pancreatic metastasis from lung cancer, particularly that which is not detected by CT alone.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / secondary. Fluorodeoxyglucose F18. Lung Neoplasms / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / secondary. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods


7. Lopez-Tomassetti Fernandez EM, Luis HD, Malagon AM, Gonzalez IA, Pallares AC: Recurrence of inflammatory pseudotumor in the distal bile duct: lessons learned from a single case and reported cases. World J Gastroenterol; 2006 Jun 28;12(24):3938-43
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  • [Title] Recurrence of inflammatory pseudotumor in the distal bile duct: lessons learned from a single case and reported cases.
  • Immunohistochemical study of these lesions limited to the pancreatic head or distal bile duct seems to be compatible with those observed in a new entity called autoimmune pancreatitis, but usually intense fibrotic reaction (zonation) predominates producing a mass.
  • When this condition is limited to the pancreatic head, the common bile duct might be involved by the inflammatory process and jaundice may occur often resembling adenocarcinoma of the pancreas.
  • We have previously reported a case of IMT arising from the bile duct associated with autoimmune pancreatitis which is an extremely rare entity.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Granuloma, Plasma Cell / pathology. Neoplasm Recurrence, Local / pathology

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  • [Cites] Clin Rheumatol. 2003 Dec;22(6):467-71 [14677031.001]
  • [Cites] JOP. 2005 Sep;6(5):455-9 [16186668.001]
  • [Cites] Clin Gastroenterol Hepatol. 2003 Nov;1(6):453-64 [15017645.001]
  • [Cites] Am J Surg Pathol. 2004 Sep;28(9):1193-203 [15316319.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):573-81 [10702209.001]
  • [Cites] N Engl J Med. 2001 Mar 8;344(10):732-8 [11236777.001]
  • [Cites] Thorac Cardiovasc Surg. 2001 Apr;49(2):124-6 [11339451.001]
  • [Cites] Pathol Res Pract. 2001;197(4):237-44 [11358009.001]
  • [Cites] Hepatogastroenterology. 2001 Jul-Aug;48(40):1118-23 [11490814.001]
  • [Cites] J Am Coll Surg. 2002 Apr;194(4):502-6 [11949755.001]
  • [Cites] Pathologe. 2002 Mar;23(2):161-6 [12001534.001]
  • [Cites] Gut. 2003 May;52(5):683-7 [12692053.001]
  • [Cites] Radiology. 2003 Jun;227(3):758-63 [12728186.001]
  • [Cites] Surg Today. 2003;33(9):714-7 [12928854.001]
  • [Cites] J Clin Pathol. 2003 Sep;56(9):715-7 [12944561.001]
  • [Cites] J Gastroenterol. 2003;38(10):982-4 [14614606.001]
  • [Cites] JOP. 2004 Sep;5(5):360-7 [15365204.001]
  • [Cites] Am J Gastroenterol. 2004 Oct;99(10):2038-40 [15447769.001]
  • [Cites] N Engl J Med. 1983 Jan 13;308(2):86-8 [6847938.001]
  • [Cites] South Med J. 1983 May;76(5):647-9 [6844969.001]
  • [Cites] Am J Gastroenterol. 1990 Feb;85(2):203-6 [2405646.001]
  • [Cites] Hum Pathol. 1991 Apr;22(4):387-95 [2050373.001]
  • [Cites] Am J Surg Pathol. 1991 Dec;15(12):1146-56 [1746682.001]
  • [Cites] Arch Pathol Lab Med. 1993 Sep;117(9):921-6 [8368906.001]
  • [Cites] Dig Dis Sci. 1995 Apr;40(4):752-6 [7720466.001]
  • [Cites] Am J Gastroenterol. 1995 Jul;90(7):1155-8 [7611217.001]
  • [Cites] Am J Surg Pathol. 1995 Aug;19(8):859-72 [7611533.001]
  • [Cites] Hum Pathol. 1995 Oct;26(10):1093-8 [7557942.001]
  • [Cites] Ital J Gastroenterol. 1995 Jun;27(5):252-5 [8541577.001]
  • [Cites] Pathology. 1995 Jul;27(3):284-8 [8532398.001]
  • [Cites] Cancer. 1996 Feb 15;77(4):778-84 [8616772.001]
  • [Cites] Am J Surg Pathol. 1996 Jun;20(6):747-53 [8651355.001]
  • [Cites] Cancer. 1995 Nov 1;76(9):1545-9 [8635056.001]
  • [Cites] Hum Pathol. 1996 Oct;27(10):1095-8 [8892598.001]
  • [Cites] Am J Surg Pathol. 1997 Oct;21(10):1166-72 [9331288.001]
  • [Cites] Pancreas. 2005 Nov;31(4):420-3 [16258381.001]
  • [Cites] Endoscopy. 2005 Nov;37(11):1127-30 [16281144.001]
  • [Cites] Pancreatology. 2006;6(1-2):145-54 [16354963.001]
  • [Cites] Pathol Res Pract. 1997;193(7):519-25; discussion 526 [9342759.001]
  • [Cites] Radiology. 1998 Feb;206(2):511-8 [9457206.001]
  • [Cites] Am J Surg Pathol. 1998 Apr;22(4):412-8 [9537467.001]
  • [Cites] Lancet. 1999 Jul 3;354(9172):43-4 [10406367.001]
  • [Cites] AJR Am J Roentgenol. 1999 Oct;173(4):1049-54 [10511176.001]
  • [Cites] Am J Surg Pathol. 2005 Feb;29(2):275-8 [15644785.001]
  • [Cites] JOP. 2005 Jan;6(1 Suppl):97-101 [15650292.001]
  • [Cites] World J Gastroenterol. 2005 Feb 14;11(6):922-5 [15682495.001]
  • [Cites] Histopathology. 2005 Aug;47(2):147-58 [16045775.001]
  • [Cites] Hum Pathol. 2005 Jul;36(7):710-7 [16084938.001]
  • [Cites] Virchows Arch. 2004 Feb;444(2):119-26 [14722765.001]
  • (PMID = 16804988.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
  • [Number-of-references] 52
  • [Other-IDs] NLM/ PMC4087951
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8. Erkan M, Kleeff J, Esposito I, Giese T, Ketterer K, Büchler MW, Giese NA, Friess H: Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis. Oncogene; 2005 Jun 23;24(27):4421-32
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  • [Title] Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis.
  • Altered expression of apoptosis-regulating genes plays an important role in the aggressive growth behavior and chemoresistance of pancreatic ductal adenocarcinoma.
  • In the present study, the hypoxia-inducible proapoptotic gene, BNIP3, was analysed in terms of expression, effect on patient survival, and chemo-responsiveness in pancreatic cancer cell lines. cDNA microarray, real-time light cycler quantitative polymerase chain reaction, laser-capture microdissection, and immunohistochemistry analyses were used to evaluate BNIP3 expression in normal and diseased pancreatic specimens.
  • The effect of chemotherapeutic agents on pancreatic cancer cells was assessed utilizing 3-(4,5-methylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromide assays.
  • BNIP3 mRNA levels were 3.0- and 6.3-fold lower in chronic pancreatitis and pancreatic cancer compared to the normal pancreas, respectively.
  • Microdissection analysis confirmed the reduction of BNIP3 expression in pancreatic cancer cells compared to normal duct cells.
  • By immunohistochemistry, BNIP3 was predominantly expressed in the acinar cells of the normal and diseased pancreas.
  • Interestingly, while BNIP3 was undetectable in the cancer cells of 59% of the cases, 75-100% of PanIN2/3 lesions displayed BNIP3 immunoreactivity.
  • Hypoxia induced BNIP3 expression in four out of eight pancreatic cancer cell lines, while it was absent under normoxic and hypoxic conditions in the remaining four.
  • In conclusion, loss of BNIP3 expression occurs late in pancreatic cancer, contributes to resistance to chemotherapy, and correlates with a worsened prognosis.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Membrane Proteins / deficiency. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / deficiency. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Fluorouracil / pharmacology. Humans. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Survival Rate

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  • (PMID = 15856026.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNIP3 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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9. Watanabe H, Okada G, Ohtsubo K, Yamaguchi Y, Mouri H, Motoo Y, Wakabayashi T, Sawabu N: Expression of mesothelin mRNA in pure pancreatic juice from patients with pancreatic carcinoma, intraductal papillary mucinous neoplasm of the pancreas, and chronic pancreatitis. Pancreas; 2005 May;30(4):349-54
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  • [Title] Expression of mesothelin mRNA in pure pancreatic juice from patients with pancreatic carcinoma, intraductal papillary mucinous neoplasm of the pancreas, and chronic pancreatitis.
  • OBJECTIVES: In the gene expression analysis of pancreatic carcinoma (PCa) using serial analysis of gene expression (SAGE) according to Ryu et al, the tag for the mesothelin mRNA transcript was present in 7 of 8 SAGE libraries derived from PCa but not in the 2 SAGE libraries derived from normal pancreatic duct epithelial cells.
  • Mesothelin mRNA expression was confirmed with in situ hybridization in all 4 resected primary PCa tumors and with RT-PCR in 18 of 20 PCa cell lines, whereas mesothelin protein expression was confirmed with immunohistochemistry in all 60 resected primary PCa tissues by Argani et al.
  • We evaluated mesothelin mRNA expression in pure pancreatic juice (PPJ) obtained from patients with PCa, chronic pancreatitis (CP), and intraductal papillary mucinous neoplasm (IPMN) of the pancreas.
  • Quantitative detection of mesothelin mRNA in PPJ may have potential diagnostic implications for pancreatic tumors.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Carcinoma, Papillary / diagnosis. Membrane Glycoproteins / genetics. Pancreatic Neoplasms / diagnosis. Pancreatitis, Chronic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Biomarkers, Tumor / genetics. Cell Line, Tumor. Female. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Molecular Sequence Data. Pancreatic Juice / physiology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15841046.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / mesothelin
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10. Ogata S, Kimura A, Hatsuse K, Yamamoto J, Shimazaki H, Nakanishi K, Kawai T: Poorly differentiated adenocarcinoma with signet-ring cell carcinoma of the extrahepatic bile duct in a 42-year-old Japanese female: a case report. Acta Med Okayama; 2010 Feb;64(1):63-5
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  • [Title] Poorly differentiated adenocarcinoma with signet-ring cell carcinoma of the extrahepatic bile duct in a 42-year-old Japanese female: a case report.
  • Poorly differentiated adenocarcinoma without papilla or tubule formation of the extrahepatic bile duct is rare.
  • Imaging studies revealed a bile duct tumor obstructing the common bile duct and invading the surrounding tissues.
  • Pathologic examination revealed a dense periductal growth of poorly differentiated adenocarcinoma containing signet-ring cells, but without papilla or tubule formation in the extrahepatic bile duct.
  • The tumor cells directly invaded the pancreatic parenchyma and the portal vein.
  • In the extrahepatic bile duct, poorly differentiated adenocarcinoma may be established as a distinct clinicopathologic entity if the tumors are characterized by:.
  • [MeSH-major] Adenocarcinoma / pathology. Bile Duct Neoplasms / pathology. Bile Ducts, Extrahepatic / pathology. Carcinoma, Signet Ring Cell / pathology

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  • (PMID = 20200586.001).
  • [ISSN] 0386-300X
  • [Journal-full-title] Acta medica Okayama
  • [ISO-abbreviation] Acta Med. Okayama
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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11. Vosters O, Beuneu C, Goldman M, Verhasselt V: N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells. Pancreas; 2008 May;36(4):363-8
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  • [Title] N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells.
  • OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion.
  • In this article, we investigated whether a salt derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement.
  • METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line.
  • To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction.
  • CONCLUSIONS: Our data suggest that Nacystelyn could be considered as a useful tool to prevent immune and inflammatory responses in pancreatic disorders by interfering with the CD40 pathway in pancreatic duct cells.
  • [MeSH-major] Acetylcysteine / analogs & derivatives. Acetylcysteine / pharmacology. Antigens, CD40 / antagonists & inhibitors. Antigens, CD40 / genetics. Inflammation / prevention & control. Lysine / analogs & derivatives. Pancreatic Ducts / physiopathology
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. NF-kappa B / drug effects. NF-kappa B / genetics. Pancreatic Neoplasms / pathology. Transcription, Genetic / drug effects

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  • (PMID = 18437082.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / N-acetylcysteine lysinate; 0 / NF-kappa B; K3Z4F929H6 / Lysine; WYQ7N0BPYC / Acetylcysteine
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12. Lowe AW, Olsen M, Hao Y, Lee SP, Taek Lee K, Chen X, van de Rijn M, Brown PO: Gene expression patterns in pancreatic tumors, cells and tissues. PLoS One; 2007 Mar 28;2(3):e323
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  • [Title] Gene expression patterns in pancreatic tumors, cells and tissues.
  • BACKGROUND: Cancers of the pancreas originate from both the endocrine and exocrine elements of the organ, and represent a major cause of cancer-related death.
  • This study provides a comprehensive assessment of gene expression for pancreatic tumors, the normal pancreas, and nonneoplastic pancreatic disease.
  • METHODS/RESULTS: DNA microarrays were used to assess the gene expression for surgically derived pancreatic adenocarcinomas, islet cell tumors, and mesenchymal tumors.
  • The addition of normal pancreata, isolated islets, isolated pancreatic ducts, and pancreatic adenocarcinoma cell lines enhanced subsequent analysis by increasing the diversity in gene expression profiles obtained.
  • Similarities in gene expression support the pancreatic duct as the origin of adenocarcinomas.
  • In addition, genes highly expressed in other cancers and associated with specific signal transduction pathways were also found in pancreatic tumors.

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  • [Cites] Ann Surg. 1999 Dec;230(6):767-74; discussion 774-5 [10615931.001]
  • [Cites] Clin Cancer Res. 2003 Dec 1;9(16 Pt 1):5988-95 [14676124.001]
  • [Cites] Nat Biotechnol. 2000 Apr;18(4):457-9 [10748532.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Sep;29(1):83-7 [10918398.001]
  • [Cites] Endocr Relat Cancer. 2004 Jun;11(2):295-303 [15163304.001]
  • [Cites] J Mol Biol. 2004 Jul 16;340(4):783-95 [15223320.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6152-8 [15448002.001]
  • [Cites] Mol Cell Biol. 1991 Oct;11(10):5016-31 [1656220.001]
  • [Cites] Br J Cancer. 1996 Apr;73(8):972-8 [8611434.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1998 Mar;34(3):211-6 [9557938.001]
  • [Cites] Genes Chromosomes Cancer. 1998 May;22(1):50-6 [9591634.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Thyroid. 1999 Jun;9(6):563-7 [10411118.001]
  • [Cites] Genomics. 1999 Aug 1;59(3):275-81 [10444328.001]
  • [Cites] Biostatistics. 2005 Jan;6(1):45-58 [15618527.001]
  • [Cites] Mol Cancer. 2005 Feb 3;4(1):9 [15691381.001]
  • [Cites] Genome Biol. 2005;6(3):R22 [15774023.001]
  • [Cites] J Cell Physiol. 2005 Jul;204(1):36-44 [15605394.001]
  • [Cites] PLoS Biol. 2005 Jun;3(6):e187 [15869330.001]
  • [Cites] Neoplasia. 2005 Jun;7(6):556-62 [16036106.001]
  • [Cites] PLoS Genet. 2006 Jan;2(1):e11 [16415983.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Nucleic Acids Res. 2001 Jan 1;29(1):152-5 [11125075.001]
  • [Cites] J Mol Biol. 2001 Jan 19;305(3):567-80 [11152613.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4320-4 [11389052.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4923-32 [11406572.001]
  • [Cites] Gastroenterology. 2001 Sep;121(3):657-67 [11522750.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476.001]
  • [Cites] Am J Pathol. 2002 Jan;160(1):91-9 [11786403.001]
  • [Cites] Mol Cell Biol. 2002 Feb;22(4):1172-83 [11809808.001]
  • [Cites] Mol Cell Biol. 2002 Feb;22(4):1184-93 [11809809.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):819-26 [11830538.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1745-54 [12000726.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421.001]
  • [Cites] Diabetes Technol Ther. 2002;4(1):67-76 [12017423.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21657-65 [11940574.001]
  • [Cites] Mol Biol Cell. 2002 Jun;13(6):1929-39 [12058060.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16203-8 [12456890.001]
  • [Cites] Nucleic Acids Res. 2003 Jan 1;31(1):219-23 [12519986.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1151-62 [12651607.001]
  • [Cites] Ann Surg Oncol. 2003 Apr;10(3):284-90 [12679314.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2649-57 [12750293.001]
  • [Cites] Ann Oncol. 2003 Jun;14(6):898-906 [12796028.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • (PMID = 17389914.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077097; United States / NCI NIH HHS / CA / CA77097
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Axin Protein; 0 / DNA, Neoplasm; 0 / RNA, Neoplasm; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC1824711
  • [General-notes] NLM/ Original DateCompleted: 20070726
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13. Yamaguchi T, Takahashi H, Kagawa R, Takeda R, Sakata S, Yamamoto M, Nishizaki D: Huge pseudocyst of the pancreas caused by poorly differentiated invasive ductal adenocarcinoma with osteoclast-like giant cells: report of a case. Hepatogastroenterology; 2007 Mar;54(74):599-601
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  • [Title] Huge pseudocyst of the pancreas caused by poorly differentiated invasive ductal adenocarcinoma with osteoclast-like giant cells: report of a case.
  • Under the tentative diagnosis of pancreatic pseudocyst of 22cm in diameter, a percutaneous drainage was performed.
  • At this time, abdominal computed tomography scan showed a tumor at the uncinate process of the pancreas.
  • It was histologically proven to be poorly differentiated ductal adenocarcinoma in combination with osteoclast-like giant cells.
  • The pseudocyst was considered to be due to the stenosis of the main pancreatic duct caused by carcinoma of the uncinate process.
  • Osteoclast-like giant cell tumor is a very rare neoplasm, the origin and prognosis of which still remain obscure.
  • However, it has to be considered in the differential diagnosis of cystic changes of the pancreas, especially of pseudocyst.
  • Furthermore, detailed surveys are needed in cases of pseudocyst of the pancreas without chronic pancreatitis, in order to identify small carcinoma of the pancreas.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / complications. Giant Cells. Osteoclasts. Pancreatic Neoplasms / complications. Pancreatic Pseudocyst / etiology
  • [MeSH-minor] Aged. Amylases / blood. Biomarkers, Tumor / blood. Cholangiopancreatography, Endoscopic Retrograde. Cholestasis, Extrahepatic / complications. Cholestasis, Extrahepatic / diagnosis. Cholestasis, Extrahepatic / pathology. Cholestasis, Extrahepatic / surgery. Decompression, Surgical. Diagnosis, Differential. Fatal Outcome. Follow-Up Studies. Humans. Liver Function Tests. Male. Pancreas / pathology. Pancreatectomy. Pancreatic Function Tests. Pancreatitis, Chronic / complications. Pancreatitis, Chronic / diagnosis. Pancreatitis, Chronic / pathology. Pancreatitis, Chronic / surgery. Splenectomy. Suction. Tomography, X-Ray Computed

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  • (PMID = 17523330.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.2.1.- / Amylases
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14. Ryschich E, Huszty G, Wentzensen N, Schmidt E, Knaebel HP, Encke J, Märten A, Büchler MW, Schmidt J: Effect of Flt3 ligand gene transfer in experimental pancreatic cancer. Int J Colorectal Dis; 2007 Feb;22(2):215-23
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  • [Title] Effect of Flt3 ligand gene transfer in experimental pancreatic cancer.
  • BACKGROUND: Fms-like tyrosine kinase 3 receptor (Flt3) is an important receptor expressed on the cell membrane of immature antigen-presenting cells.
  • The aim of the present study was to study the effect of FL gene transfer on the immune response and tumor growth in experimental pancreatic cancer.
  • Transfection efficiency of subcutaneously growing rat duct-like pancreatic cancer (DSL6A) with DOTAP-/cholesterol-based liposomes was tested using a pcDNA3.1-lacZ construct.
  • Tumor induction was achieved in Lewis rats by a subcutaneous inoculation of syngeneic pancreatic tumor cells (DSL6A).
  • [MeSH-major] Adenocarcinoma / immunology. Membrane Proteins / immunology. Pancreatic Neoplasms / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Dendritic Cells / immunology. Gene Transfer Techniques. Immunotherapy. Killer Cells, Natural / immunology. Male. Molecular Sequence Data. Neoplasms, Experimental. Rats. Rats, Inbred Lew. Sequence Analysis, DNA

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  • [Cites] Int J Cancer. 2000 Jun 15;86(6):827-34 [10842197.001]
  • [Cites] J Immunol. 1998 Sep 15;161(6):2817-24 [9743341.001]
  • [Cites] Cancer Res. 2000 Apr 15;60(8):2081-4 [10786663.001]
  • [Cites] Lancet Oncol. 2004 Sep;5(9):541-9 [15337483.001]
  • [Cites] Cancer Res. 1998 Feb 1;58(3):380-3 [9458075.001]
  • [Cites] J Immunother. 2004 Jan-Feb;27(1):13-26 [14676630.001]
  • [Cites] Hum Gene Ther. 1999 Sep 1;10(13):2141-51 [10498246.001]
  • [Cites] Cancer Gene Ther. 2003 Feb;10(2):96-104 [12536197.001]
  • [Cites] Cancer Immunol Immunother. 2004 Nov;53(11):946-54 [15185012.001]
  • [Cites] Cancer Immunol Immunother. 2002 Dec;51(11-12):669-73 [12439613.001]
  • [Cites] Ann Surg. 2003 Jan;237(1):74-85 [12496533.001]
  • [Cites] Am J Pathol. 1993 Jul;143(1):292-303 [8391218.001]
  • [Cites] J Exp Med. 2003 Jul 21;198(2):305-13 [12874263.001]
  • [Cites] Gynecol Oncol. 2000 Jun;77(3):377-82 [10831345.001]
  • [Cites] Cytokine. 2000 Feb;12(2):87-100 [10671293.001]
  • [Cites] J Immunol. 1998 Dec 1;161(11):6164-70 [9834102.001]
  • [Cites] Minerva Chir. 2004 Apr;59(2):99-111 [15238885.001]
  • [Cites] Nat Med. 1997 Jun;3(6):625-31 [9176488.001]
  • [Cites] Oncogene. 1995 Jan 5;10(1):149-57 [7824267.001]
  • [Cites] Am J Surg. 2000 May;179(5):367-71 [10930481.001]
  • [Cites] Cancer Immunol Immunother. 2003 Sep;52(9):535-45 [14627125.001]
  • [Cites] Nat Immunol. 2004 Jan;5(1):7-10 [14699398.001]
  • [Cites] J Clin Invest. 2004 Mar;113(5):774-83 [14991076.001]
  • [Cites] Annu Rev Immunol. 2002;20:621-67 [11861614.001]
  • [Cites] J Immunother. 2002 Jan-Feb;25(1):27-35 [11924908.001]
  • [Cites] J Exp Med. 2001 Jan 15;193(2):233-8 [11208863.001]
  • [Cites] Cancer Gene Ther. 2004 Nov;11(11):733-9 [15486560.001]
  • [Cites] J Exp Med. 1996 Nov 1;184(5):1953-62 [8920882.001]
  • [Cites] Int J Cancer. 2001 May 1;92(3):441-50 [11291084.001]
  • [Cites] Pancreas. 2003 Mar;26(2):166-72 [12604915.001]
  • [Cites] Cancer Biol Ther. 2002 Sep-Oct;1(5):486-9 [12496473.001]
  • [Cites] Surg Oncol Clin N Am. 2004 Oct;13(4):663-74, ix [15350940.001]
  • [Cites] Cancer Res. 1997 Aug 15;57(16):3511-6 [9270021.001]
  • [Cites] Cancer Res. 1999 Dec 15;59(24):6028-32 [10626784.001]
  • [Cites] Blood. 1996 Sep 15;88(6):2004-12 [8822919.001]
  • [Cites] J Exp Med. 1994 Nov 1;180(5):1849-60 [7525841.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8998-9002 [2461560.001]
  • [Cites] Leukemia. 1999 Aug;13(8):1188-99 [10450746.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Ann Surg. 2001 Dec;234(6):758-68 [11729382.001]
  • [Cites] Int J Gastrointest Cancer. 2002;32(1):1-6 [12630764.001]
  • [Cites] Int J Oncol. 2003 Feb;22(2):345-51 [12527933.001]
  • [Cites] Zhonghua Yi Xue Za Zhi. 2002 Jun 10;82(11):775-9 [12126551.001]
  • [Cites] J Immunol. 1999 Aug 1;163(3):1289-97 [10415026.001]
  • [Cites] J Immunol. 2003 Apr 1;170(7):3554-64 [12646617.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):498-504 [15701833.001]
  • [Cites] Cancer Res. 1997 Jul 1;57(13):2681-6 [9205077.001]
  • [Cites] Int J Cancer. 2003 Dec 10;107(5):773-80 [14566827.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3 Suppl):925s-932s [11300493.001]
  • (PMID = 16528542.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / flt3 ligand protein
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15. Hassan R, Laszik ZG, Lerner M, Raffeld M, Postier R, Brackett D: Mesothelin is overexpressed in pancreaticobiliary adenocarcinomas but not in normal pancreas and chronic pancreatitis. Am J Clin Pathol; 2005 Dec;124(6):838-45
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  • [Title] Mesothelin is overexpressed in pancreaticobiliary adenocarcinomas but not in normal pancreas and chronic pancreatitis.
  • Mesothelin, a cell surface glycoprotein present on normal mesothelial cells, has been reported to be expressed in pancreatic adenocarcinomas.
  • We conducted this study to fully characterize mesothelin expression in surgically resected, formalin-fixed, paraffin-embedded tissue specimens of 18 pancreatic adenocarcinomas, 9 adenocarcinomas of the ampulla of Vater, 12 adenocarcinomas of the common bile duct, and 17 cases of chronic pancreatitis.
  • All 18 cases (100%) of pancreatic adenocarcinomas showed mesothelin expression, as did 8 (89%) of 9 cases of ampullar adenocarcinoma and all 12 cases (100%) of common bile duct adenocarcinoma.
  • In all cases of pancreaticobiliary adenocarcinoma, the adjacent normal pancreas did not stain for mesothelin.
  • Of 17 specimens of chronic pancreatitis, 16 were negative for mesothelin expression, and 1 case showed weak mesothelin staining of fewer than 5% of normal pancreatic ducts.
  • Our results demonstrated mesothelin expression in the majority of pancreaticobiliary adenocarcinomas and no expression in normal pancreatic tissues and in chronic pancreatitis.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Membrane Glycoproteins / biosynthesis. Pancreatic Neoplasms / metabolism. Pancreatitis, Chronic / metabolism
  • [MeSH-minor] Common Bile Duct / metabolism. Common Bile Duct / pathology. GPI-Linked Proteins. Humans. Immunohistochemistry. Pancreas / metabolism

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  • (PMID = 16416732.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / mesothelin
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16. Bernstein C, Bernstein H, Payne CM, Dvorak K, Garewal H: Field defects in progression to gastrointestinal tract cancers. Cancer Lett; 2008 Feb 18;260(1-2):1-10
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  • However, field defects are often overlooked in studies of cancer progression through assuming tissue at some distance from the cancer is normal.
  • We indicate, however, the generality of field defects in gastrointestinal cancers, including cancers of the oropharynx, esophagus, stomach, bile duct, pancreas, small intestine and colon/rectum.
  • These features are often associated with high bile acid exposure and may explain the association of dietary-related factors with cancer progression.

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  • [Cites] Br J Cancer. 1991 Jan;63(1):143-5 [1989654.001]
  • [Cites] Environ Health Perspect. 1993 Mar;99:169-73 [8319616.001]
  • [Cites] Carcinogenesis. 1994 Jul;15(7):1459-62 [8033325.001]
  • [Cites] Am J Pathol. 1995 Jan;146(1):20-6 [7856728.001]
  • [Cites] Ultrastruct Pathol. 1995 Jul-Aug;19(4):221-48 [7571081.001]
  • [Cites] Cancer Res. 1996 Apr 1;56(7):1480-3 [8603388.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1237-40 [8640805.001]
  • [Cites] Laryngoscope. 1998 Feb;108(2):250-6 [9473077.001]
  • [Cites] Int J Cancer. 1998 Nov 23;78(5):568-75 [9808524.001]
  • [Cites] Oral Oncol. 1998 Jul;34(4):270-5 [9813722.001]
  • [Cites] Gut. 1999 May;44(5):598-602 [10205192.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2353-7 [10344743.001]
  • [Cites] Oral Oncol. 1999 Mar;35(2):157-63 [10435150.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2004;11(5):301-9 [15549428.001]
  • [Cites] Dis Esophagus. 2004;17(4):322-7 [15569371.001]
  • [Cites] Mutat Res. 2005 Jan;589(1):47-65 [15652226.001]
  • [Cites] Am J Gastroenterol. 2005 Feb;100(2):424-31 [15667503.001]
  • [Cites] Curr Opin Gastroenterol. 2005 Jan;21(1):32-8 [15687882.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1400-7 [15746039.001]
  • [Cites] Cancer Lett. 2005 Jul 8;225(1):53-9 [15922857.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):2054-65 [15940637.001]
  • [Cites] Carcinogenesis. 2005 Sep;26(9):1513-9 [15860506.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2113-7 [16172218.001]
  • [Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1330-8 [16174854.001]
  • [Cites] J Surg Oncol. 2005 Dec 1;92(3):169-90 [16299787.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):714-9 [16407113.001]
  • [Cites] World J Gastroenterol. 2006 Jan 21;12(3):354-62 [16489633.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):107-16 [16491070.001]
  • [Cites] Inflamm Bowel Dis. 2006 Apr;12(4):278-93 [16633050.001]
  • [Cites] J Gastroenterol. 2006 May;41(5):401-7 [16799880.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6553-62 [16818627.001]
  • [Cites] J Clin Pathol. 2006 Sep;59(9):942-6 [16679352.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2317-21 [17119066.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18238-42 [17108085.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):22-32 [16713672.001]
  • [Cites] Histopathology. 2007 Jan;50(2):203-9 [17222248.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2007;21(2):281-97 [17382277.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Jun;46(6):532-42 [17330261.001]
  • [Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S49-60 [17486052.001]
  • [Cites] Gut. 2007 Jun;56(6):763-71 [17145738.001]
  • [Cites] Am J Epidemiol. 2007 Jun 15;165(12):1424-33 [17420181.001]
  • [Cites] JAMA. 2007 Aug 15;298(7):754-64 [17699009.001]
  • [Cites] Cancer Res. 1999 Oct 15;59(20):5148-53 [10537290.001]
  • [Cites] Nature. 2000 Mar 23;404(6776):398-402 [10746728.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Mar;9(3):249-56 [10750662.001]
  • [Cites] Gut. 2000 May;46(5):645-50 [10764707.001]
  • [Cites] Cancer Res. 2000 Jul 15;60(14):3893-8 [10919665.001]
  • [Cites] Gut. 2001 Feb;48(2):238-46 [11156647.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3573-7 [11325821.001]
  • [Cites] Mod Pathol. 2001 May;14(5):397-403 [11353048.001]
  • [Cites] Gastroenterology. 2001 Dec;121(6):1286-93 [11729107.001]
  • [Cites] Cancer. 2001 Oct 1;92(7):1807-17 [11745253.001]
  • [Cites] Gastric Cancer. 2002;5(1):16-22 [12021855.001]
  • [Cites] Ann Surg Oncol. 2002 Jun;9(5):505-17 [12052764.001]
  • [Cites] Scand J Gastroenterol. 2002 Oct;37(10):1205-11 [12408527.001]
  • [Cites] Gastroenterology. 2002 Dec;123(6):2052-63 [12454861.001]
  • [Cites] J Pathol. 2003 Mar;199(3):354-60 [12579537.001]
  • [Cites] Chem Biol Interact. 2003 Mar 6;145(1):53-66 [12606154.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1727-30 [12702551.001]
  • [Cites] Helicobacter. 2003 Jun;8(3):227-34 [12752735.001]
  • [Cites] Carcinogenesis. 2004 Mar;25(3):419-23 [14656949.001]
  • [Cites] Clin Cancer Res. 2004 Mar 15;10(6):2020-8 [15041721.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3694-700 [15150130.001]
  • [Cites] Cancer Res. 1988 Jan 15;48(2):483-9 [3335016.001]
  • [Cites] Lancet. 1988 May 21;1(8595):1149-51 [2896968.001]
  • [Cites] Lancet. 1989 Sep 30;2(8666):783-5 [2571019.001]
  • [Cites] Cancer Genet Cytogenet. 1989 Oct 15;42(2):281-6 [2790761.001]
  • [Cites] J Cancer Res Clin Oncol. 1989;115(5):423-8 [2808479.001]
  • (PMID = 18164807.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095060-01; United States / NCI NIH HHS / CA / R21CA111513-01A1; United States / NCI NIH HHS / CA / CA095060-06A1; United States / NCI NIH HHS / CA / 5 R01 CA119087; United States / NCI NIH HHS / CA / R21 CA111513-02; United States / NCI NIH HHS / CA / CA111513-01A1; United States / NCI NIH HHS / CA / R01 CA119087; United States / NCI NIH HHS / CA / R21 CA111513; United States / NCI NIH HHS / CA / CA095060-04; United States / NCI NIH HHS / CA / P50 CA095060-03; United States / NCI NIH HHS / CA / CA119087-03; United States / NCI NIH HHS / CA / P50 CA095060-06A1; United States / NCI NIH HHS / CA / CA095060-01; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / CA095060-03; United States / NCI NIH HHS / CA / R21 CA111513-01A1; None / None / / P50 CA095060-05; United States / NCI NIH HHS / CA / CA119087-01A1; United States / NCI NIH HHS / CA / P50 CA095060-04; United States / NCI NIH HHS / CA / P50 CA095060-02; United States / NCI NIH HHS / CA / CA095060-02; United States / NCI NIH HHS / CA / CA119087-02; United States / NCI NIH HHS / CA / R01 CA119087-03; United States / NCI NIH HHS / CA / 1 P50 CA95060; United States / NCI NIH HHS / CA / P50 CA095060-05; United States / NCI NIH HHS / CA / R01 CA119087-02; United States / NCI NIH HHS / CA / R01 CA119087-01A1; United States / NCI NIH HHS / CA / CA111513-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Bile Acids and Salts
  • [Number-of-references] 69
  • [Other-IDs] NLM/ NIHMS39621; NLM/ PMC2744582
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17. Layfield LJ, Cramer H: Fine-needle aspiration cytology of intraductal papillary-mucinous tumors: a retrospective analysis. Diagn Cytopathol; 2005 Jan;32(1):16-20
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  • Intraductal papillary-mucinous tumor (IPMT) of the pancreas has become the accepted terminology for a group of mucin-producing epithelial proliferations lying within ectatic segments of the main pancreatic duct or its large branches.
  • Cytological specimens obtained by endoscopic ultrasound-guided or percutaneous fine-needle aspiration (FNA) are characterized by a background containing abundant mucin in which are entrapped single or loosely cohesive clusters of neoplastic cells characteristically showing a goblet-cell morphology.
  • The degree of nuclear atypia, cell crowding, and cell shape varies between smears within a single case and between cases.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Biopsy, Fine-Needle / methods. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Nucleus / pathology. Cell Shape. Endosonography. Humans. Mucins / analysis. Retrospective Studies. Staining and Labeling

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15584051.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mucins
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18. Tanaka H, Fukamachi K, Futakuchi M, Alexander DB, Long N, Tamamushi S, Minami K, Seino S, Ohara H, Joh T, Tsuda H: Mature acinar cells are refractory to carcinoma development by targeted activation of Ras oncogene in adult rats. Cancer Sci; 2010 Feb;101(2):341-6
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  • Pancreatic ductal adenocarcinoma (PDA) is one of the most debilitating malignancies in humans.
  • When adenovirus with Cre recombinase under the control of the CMV enhancer/chicken beta-actin (CAG) promoter (Ad-CAG-Cre) is injected into the pancreatic duct of these animals, pancreatic neoplasias develop.
  • Pathologically, the origin of these lesions is duct, intercalated duct, and centroacinar cells, but not acinar cells.
  • The present study was undertaken to test the effect of acinar cell-specific oncogenic ras expression.
  • Adult transgenic rats were injected with adenovirus with Cre recombinase under the control of the acinar cell-specific promoters amylase (Ad-Amy-Cre) and elastase-1 (Ad-Ela-Cre) or under the control of the non-specific CAG promoter.
  • Injection of either Ad-Amy-Cre or Ad-Ela-Cre into the pancreatic ducts of transgenic animals in which oncogenic Kras is tagged with hemagglutinin (HA), HA-Kras(G12V) rats resulted in expression of oncogenic ras in acinar cells but not in duct, intercalated duct, or centroacinar cells.
  • In marked contrast, injection of Ad-CAG-Cre resulted in pancreatic cancer development within 4 weeks.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / etiology. Genes, ras. Pancreas, Exocrine / pathology. Pancreatic Neoplasms / etiology

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  • (PMID = 19917056.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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19. Yoshida T, Shiraki N, Baba H, Goto M, Fujiwara S, Kume K, Kume S: Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas. Genes Cells; 2008 Jul;13(7):667-78
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  • [Title] Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas.
  • Here we analyzed the expression patterns of Eppk1 in the developing and adult pancreas in the mice.
  • In the embryonic pancreas, Eppk1+/Pdx1+ and Eppk1+/Sox9+ pancreatic progenitor cells were observed in early pancreatic epithelium.
  • Then Eppk1 expression becomes confined to Ngn3+ or Sox9+ endocrine progenitor cells, and p48+ exocrine progenitor cells, and then restricted to the duct cells and a cells at birth.
  • In the adult pancreas, Eppk1 is expressed in centroacinar cells (CACs) and in duct cells.
  • Eppk1 is observed in pancreatic intraepithelial neoplasia (PanIN), previously identified as pancreatic ductal adenocarcinoma (PDAC) precursor lesions.
  • In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an acinar cell regeneration model.
  • These results suggest that Eppk1 serves as a useful marker for detecting pancreatic progenitor cells in developing and regenerating pancreas.
  • [MeSH-major] Autoantigens / biosynthesis. Autoantigens / genetics. Gene Expression Regulation / physiology. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Regeneration / physiology
  • [MeSH-minor] Animals. Biomarkers / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Knockout. Mice, Transgenic. Stem Cells / cytology. Stem Cells / metabolism


20. Plentz R, Park JS, Rhim AD, Abravanel D, Hezel AF, Sharma SV, Gurumurthy S, Deshpande V, Kenific C, Settleman J, Majumder PK, Stanger BZ, Bardeesy N: Inhibition of gamma-secretase activity inhibits tumor progression in a mouse model of pancreatic ductal adenocarcinoma. Gastroenterology; 2009 May;136(5):1741-9.e6
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  • [Title] Inhibition of gamma-secretase activity inhibits tumor progression in a mouse model of pancreatic ductal adenocarcinoma.
  • BACKGROUND & AIMS: The Notch signaling pathway is required for the expansion of undifferentiated pancreatic progenitor cells during embryonic development and has been implicated in the progression of pancreatic ductal adenocarcinoma (PDAC).
  • METHODS: We tested the effects of a gamma-secretase inhibitor (GSI) that blocks Notch signaling in PDAC cell lines and a genetically engineered mouse model of PDAC (Kras p53 L/+ mice).
  • The GSI inhibited the growth of premalignant pancreatic duct-derived cells in a Notch-dependent manner.
  • Additionally, in a panel of over 400 human solid tumor-derived cell lines, PDAC cells, as a group, were more sensitive to the GSI than any other tumor type.

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  • [Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):314-22 [15665828.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):964-8 [15959516.001]
  • [Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]
  • [Cites] Genes Dev. 2005 Aug 15;19(16):1825-39 [16103211.001]
  • [Cites] Bioorg Med Chem Lett. 2005 Oct 1;15(19):4212-6 [16054361.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12443-8 [16107537.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):171-2 [16169459.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):185-95 [16169464.001]
  • [Cites] Ann Surg. 2005 Dec;242(6):791-800, discussion 800-1 [16327489.001]
  • [Cites] Mol Cancer Ther. 2006 Mar;5(3):483-93 [16546962.001]
  • [Cites] J Clin Invest. 2006 Apr;116(4):996-1004 [16543950.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5947-52 [16585505.001]
  • [Cites] Immunity. 2006 Nov;25(5):823-34 [17081781.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1032-7 [17183313.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):36-44 [10615124.001]
  • [Cites] Peptides. 2002 Jul;23(7):1285-97 [12128085.001]
  • [Cites] Nat Med. 2002 Sep;8(9):979-86 [12185362.001]
  • [Cites] Cancer Biol Ther. 2002 Nov-Dec;1(6):599-606 [12642680.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Dev Biol. 2003 Aug 15;260(2):426-37 [12921743.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2003;4:237-56 [14527303.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5 [14657333.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Pancreas. 2004 Jan;28(1):58-64 [14707731.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):250-60 [15236190.001]
  • [Cites] Development. 2004 Sep;131(17):4213-24 [15280211.001]
  • [Cites] Toxicol Sci. 2004 Nov;82(1):341-58 [15319485.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2403-13 [9196156.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3780-92 [9808572.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1083-7 [17183323.001]
  • [Cites] Nat Rev Immunol. 2007 Jan;7(1):64-75 [17170755.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1879-82 [17332312.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):211-3 [17349578.001]
  • [Cites] Am J Pathol. 2007 Jul;171(1):263-73 [17591971.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8051-7 [17804716.001]
  • [Cites] Gastroenterology. 2007 Dec;133(6):2056-9 [18054579.001]
  • [Cites] J Clin Invest. 2008 Jan;118(1):217-28 [18079963.001]
  • [Cites] Cell Mol Life Sci. 2007 Nov;64(21):2746-62 [17687513.001]
  • [Cites] Gastroenterology. 2008 Feb;134(2):544-55 [18242220.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Methods Enzymol. 2008;438:331-41 [18413259.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18913-8 [19028870.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18907-12 [19028876.001]
  • [CommentIn] Gastroenterology. 2009 May;136(5):1499-502 [19327730.001]
  • (PMID = 19208345.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5P01CA117969; United States / NCI NIH HHS / CA / 5K01CA104647; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / R01 CA133557; United States / NIDDK NIH HHS / DK / T32-DK007066; United States / NIDDK NIH HHS / DK / T32 DK007066
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic S-Oxides; 0 / MRK 003; 0 / Receptors, Notch; 0 / Thiadiazoles; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS88478; NLM/ PMC3675892
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21. Warnecke-Eberz U, Prenzel KL, Baldus SE, Metzger R, Dienes HP, Bollschweiler E, Hoelscher AH, Schneider PM: Significant down-regulation of the plasminogen activator inhibitor 1 mRNA in pancreatic cancer. Pancreas; 2008 Mar;36(2):173-7
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  • [Title] Significant down-regulation of the plasminogen activator inhibitor 1 mRNA in pancreatic cancer.
  • OBJECTIVES: We examined mRNA expression of the urokinase-type plasminogen activator (uPA), its receptor (uPAR), and the plasminogen activator inhibitor 1 (PAI-1) in a panel of adenocarcinomas of the pancreas (PC) and cancers of the papilla of Vater (CPV).
  • [MeSH-major] Adenocarcinoma / genetics. Ampulla of Vater / pathology. Common Bile Duct Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics. Plasminogen Activator Inhibitor 1 / genetics. RNA, Messenger / analysis
  • [MeSH-minor] Adult. Aged. Down-Regulation. Female. Humans. Male. Middle Aged. Prognosis. Receptors, Cell Surface / genetics. Receptors, Urokinase Plasminogen Activator. Reverse Transcriptase Polymerase Chain Reaction. Urokinase-Type Plasminogen Activator / genetics

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  • (PMID = 18376309.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PLAUR protein, human; 0 / Plasminogen Activator Inhibitor 1; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 0 / SERPINE1 protein, human; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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22. Dowen SE, Crnogorac-Jurcevic T, Gangeswaran R, Hansen M, Eloranta JJ, Bhakta V, Brentnall TA, Lüttges J, Klöppel G, Lemoine NR: Expression of S100P and its novel binding partner S100PBPR in early pancreatic cancer. Am J Pathol; 2005 Jan;166(1):81-92
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  • [Title] Expression of S100P and its novel binding partner S100PBPR in early pancreatic cancer.
  • S100P is a member of the S100 family of calcium-binding proteins and there have been several recent reports of its overexpression in pancreatic ductal adenocarcinoma (PDAC).
  • S100PBPR was found to localize to cell nuclei where S100P is also present, and the two proteins co-immunoprecipitate.
  • By in situ hybridization, S100PBPR transcript was found in islet cells but not duct cells of the healthy pancreas.
  • Both S100P and S100PBPR were detected by quantitative real-time polymerase chain reaction in pancreatic intraepithelial neoplasia (PanIN) and PDAC samples, and in situ hybridization revealed the presence of S100PBPR transcript in malignant PDAC cells.
  • These data suggest that an interaction between S100P and S100PBPR may be involved in early pancreatic cancer.
  • [MeSH-major] Calcium-Binding Proteins / genetics. Carrier Proteins / genetics. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Base Sequence. Calcium / metabolism. Cloning, Molecular. DNA Primers. Disease Progression. Humans. In Situ Hybridization. Magnesium / metabolism. Polymerase Chain Reaction. RNA, Messenger / genetics. Transfection

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  • [Cites] Oncogene. 2002 Jul 4;21(29):4587-94 [12085237.001]
  • [Cites] Am J Clin Pathol. 1994 Jun;101(6):684-8 [8209852.001]
  • [Cites] J Biol Chem. 2002 Aug 9;277(32):28848-52 [12042313.001]
  • [Cites] CA Cancer J Clin. 2003 Jan-Feb;53(1):5-26 [12568441.001]
  • [Cites] Cancer Biol Ther. 2002 Nov-Dec;1(6):607-13 [12642681.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1151-62 [12651607.001]
  • [Cites] Int J Oncol. 2000 Feb;16(2):231-40 [10639564.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):2002-6 [10766191.001]
  • [Cites] Am J Pathol. 2000 May;156(5):1767-71 [10793087.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):1821-5 [10854204.001]
  • [Cites] Biochemistry. 2000 Aug 8;39(31):9533-9 [10924150.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):2969-72 [10955772.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6134-41 [11085537.001]
  • [Cites] Am J Pathol. 2001 May;158(5):1677-83 [11337365.001]
  • [Cites] Int J Biochem Cell Biol. 2001 Jul;33(7):637-68 [11390274.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4923-32 [11406572.001]
  • [Cites] Oncogene. 2001 Nov 1;20(50):7437-46 [11704875.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8830-7 [11751405.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1256-60 [11888886.001]
  • [Cites] Verh Dtsch Ges Pathol. 2001;85:219-28 [11894402.001]
  • [Cites] Am J Pathol. 2002 Apr;160(4):1239-49 [11943709.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1745-54 [12000726.001]
  • [Cites] Cancer Res. 2002 May 15;62(10):2890-6 [12019169.001]
  • [Cites] Protein Sci. 2002 Jun;11(6):1367-75 [12021435.001]
  • [Cites] Anat Rec. 2002 May 1;267(1):60-9 [11984793.001]
  • [Cites] World J Gastroenterol. 2003 Apr;9(4):818-23 [12679940.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2649-57 [12750293.001]
  • [Cites] Mol Biol Cell. 2003 Jun;14(6):2372-84 [12808036.001]
  • [Cites] Cancer Sci. 2003 Mar;94(3):263-70 [12824920.001]
  • [Cites] Cell Mol Life Sci. 2003 Jun;60(6):1180-99 [12861384.001]
  • [Cites] J Pathol. 2003 Sep;201(1):63-74 [12950018.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2003;4:237-56 [14527303.001]
  • [Cites] Virchows Arch. 2003 Oct;443(4):508-17 [12942322.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2003 Aug;2(3):467-70 [14599962.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] J Biol Chem. 2004 Feb 13;279(7):5059-65 [14617629.001]
  • [Cites] Cancer Res. 1994 Jul 1;54(13):3568-73 [8012983.001]
  • [Cites] Am J Pathol. 1994 Dec;145(6):1291-5 [7992834.001]
  • [Cites] Hum Pathol. 1996 Feb;27(2):119-24 [8617452.001]
  • [Cites] Am J Pathol. 1996 Jun;148(6):1763-70 [8669463.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2140-3 [9187111.001]
  • [Cites] Anticancer Drugs. 1998 Apr;9(4):311-7 [9635921.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Jun;7(6):515-21 [9641496.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4740-4 [9788631.001]
  • [Cites] J Mol Biol. 1998 Oct 30;283(3):679-94 [9784376.001]
  • [Cites] Hum Pathol. 1999 Feb;30(2):123-9 [10029438.001]
  • [Cites] Cancer. 1999 Apr 15;85(8):1703-10 [10223563.001]
  • [Cites] Ann Oncol. 1999;10 Suppl 4:64-8 [10436788.001]
  • [Cites] J Exp Clin Cancer Res. 2003 Jun;22(2):307-13 [12866582.001]
  • [Cites] Oncogene. 2004 Feb 26;23(8):1531-8 [14716296.001]
  • [Cites] N Engl J Med. 2004 Mar 18;350(12):1200-10 [15028824.001]
  • [Cites] Oncogene. 2004 Mar 25;23(13):2385-400 [14767473.001]
  • [Cites] N Engl J Med. 1992 Feb 13;326(7):455-65 [1732772.001]
  • [Cites] Eur J Biochem. 1992 Jul 15;207(2):541-7 [1633809.001]
  • [Cites] Am J Pathol. 1994 May;144(5):889-95 [8178941.001]
  • [Cites] Nat Med. 2002 Aug;8(8):816-24 [12118244.001]
  • (PMID = 15632002.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Carrier Proteins; 0 / DNA Primers; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / S100P protein, human; 0 / S100PBP protein, human; I38ZP9992A / Magnesium; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC1602285
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23. Suzuki S, Tanaka S, Hayashi T, Harada N, Suzuki M, Hanyu F, Ban S: Small-cell neuroendocrine carcinoma of the ampulla of Vater. J Hepatobiliary Pancreat Surg; 2006;13(5):450-3
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  • [Title] Small-cell neuroendocrine carcinoma of the ampulla of Vater.
  • We report a patient (an 80-year-old woman) with anemia and fecal occult blood, who had an emergency operation for carcinoma of the cecum (well-differentiated adenocarcinoma without local lymph node metastasis).
  • Histology of the resected tumor was that of small-cell carcinoma, and immunohistochemistry showed positive staining for neuron-specific enolase, chromogranin A, and synaptophysin, confirming the neuroendocrine nature of the tumor.
  • As the histology of the tumor was distinct from cecal carcinoma, and no tumors were found in other organs, the tumor was diagnosed as primary small-cell neuroendocrine carcinoma of the ampulla of Vater.
  • [MeSH-major] Ampulla of Vater. Carcinoma, Neuroendocrine / pathology. Carcinoma, Small Cell / pathology. Common Bile Duct Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Aged, 80 and over. Cecal Neoplasms / pathology. Female. Humans. Neoplasms, Multiple Primary. Pancreaticoduodenectomy

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  • (PMID = 17013721.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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24. Agbunag C, Lee KE, Buontempo S, Bar-Sagi D: Pancreatic duct epithelial cell isolation and cultivation in two-dimensional and three-dimensional culture systems. Methods Enzymol; 2006;407:703-10
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  • [Title] Pancreatic duct epithelial cell isolation and cultivation in two-dimensional and three-dimensional culture systems.
  • Pancreatic ductal adenocarcinoma (PDA) is generally considered to have originated from pancreatic duct epithelial cells (PDEC).
  • The availability of these culture systems should be particularly useful for studying their relationships between specific genetic lesions and the morphogenic changes that accompany pancreatic ductal tumorigenesis.
  • [MeSH-major] Cell Culture Techniques / methods. Pancreatic Ducts / cytology
  • [MeSH-minor] Animals. Cell Separation. Epithelial Cells / cytology. Fluorescent Antibody Technique. Mice. Rats

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  • (PMID = 16757363.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Sadakari Y, Ienaga J, Kobayashi K, Miyasaka Y, Takahata S, Nakamura M, Mizumoto K, Tanaka M: Cyst size indicates malignant transformation in branch duct intraductal papillary mucinous neoplasm of the pancreas without mural nodules. Pancreas; 2010 Mar;39(2):232-6
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  • [Title] Cyst size indicates malignant transformation in branch duct intraductal papillary mucinous neoplasm of the pancreas without mural nodules.
  • OBJECTIVES: In branch duct intraductal papillary mucinous neoplasm (IPMN) of the pancreas, the importance of the cyst size to predict malignancy is still controversial.
  • Our aim was to elucidate the malignant potential of branch duct IPMN without mural nodules (flat branch duct IPMN).
  • METHODS: Seventy-three patients with flat branch duct IPMNs were studied in our institution.
  • Statistically significant predictors of malignancy were atypical cytological condition and main pancreatic duct (MPD) diameter of 5 mm or more.
  • The frequency of malignancy in flat branch duct IPMNs with the size of 30 mm or more and MPD diameter of less than 5 mm was 3.6%, whereas there were 5 malignant cases (26.3%) in flat branch duct IPMNs with the size of 30 mm or more and MPD diameter of 5 mm or more.
  • CONCLUSIONS: We conclude that the size criteria (> or =30 mm) to predict malignancy proposed in the international consensus guidelines is appropriate and resection or meticulous follow-up using cytological examination and MPD dilatation is needed in patients with flat branch duct IPMNs.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Papillary / pathology. Carcinoma, Pancreatic Ductal / pathology. Cell Transformation, Neoplastic / pathology. Pancreatic Cyst / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 19752768.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Aloysius MM, Hewavisenthi SJ, Bates TE, Rowlands BJ, Lobo DN, Zaitoun AM: Predictive value of tumor proliferative indices in periampullary cancers: Ki-67, mitotic activity index (MI) and volume corrected mitotic index (M/V) using tissue microarrays. World J Surg; 2010 Sep;34(9):2115-21
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  • METHODS: Immunohistochemical staining for Ki-67 was performed on formalin-fixed pancreatic TMA sections.
  • Expression of Ki-67 was assessed as the percentage of cancer cell nuclei expressing MIB1, MI as the mean percentage of Ki-67 from 10 random high-power fields, and M/V was calculated after standardizing MI for connective tissue volume and microscope parameters in the tumor using established protocols.
  • The median survival for tumors of the pancreaticobiliary subtype (pancreatic ductal adenocarcinoma and cholangiocarcinoma) was 43 months in the group with an M/V score of <20, compared with 18 months for the group with a score > or =20 (P = 0.001).
  • There was no statistically significant difference in survival, based on M/V score, for tumors of the intestinal subtype (ampullary and duodenal adenocarcinoma).
  • [MeSH-major] Ampulla of Vater. Bile Duct Neoplasms / metabolism. Bile Ducts, Intrahepatic. Carcinoma, Pancreatic Ductal / metabolism. Cholangiocarcinoma / metabolism. Common Bile Duct Neoplasms / metabolism. Duodenal Neoplasms / metabolism. Ki-67 Antigen / analysis. Mitotic Index. Pancreatic Neoplasms / metabolism

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  • [Cites] Cancer. 1993 Apr 1;71(7):2191-9 [8384065.001]
  • [Cites] Tohoku J Exp Med. 1995 Dec;177(4):375-7 [8928197.001]
  • [Cites] Br J Cancer. 2000 Jan;82(2):381-4 [10646892.001]
  • [Cites] Scand J Gastroenterol. 1990 Jun;25(6):548-54 [2359985.001]
  • [Cites] Scand J Gastroenterol. 1991 May;26(5):483-90 [1651557.001]
  • [Cites] BMC Cancer. 2009 Sep 15;9:327 [19754967.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2000;7(5):489-95 [11180876.001]
  • [Cites] Mod Pathol. 2000 Dec;13(12):1300-7 [11144926.001]
  • [Cites] Pol J Pathol. 2009;60(3):124-9 [20069505.001]
  • [Cites] Histopathology. 1993 Apr;22(4):355-60 [8514278.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2002;9(1):1-11 [12021893.001]
  • [Cites] Histopathology. 2009 Aug;55(2):236-7 [19694833.001]
  • [Cites] J Natl Cancer Inst. 2009 Jan 21;101(2):114-9 [19141773.001]
  • [Cites] Clin Cancer Res. 1998 Nov;4(11):2605-14 [9829723.001]
  • [Cites] Hum Pathol. 1996 Nov;27(11):1124-34 [8912819.001]
  • [Cites] J Am Coll Surg. 2008 Aug;207(2):210-8 [18656049.001]
  • [Cites] BMC Cancer. 2008 Jun 11;8:170 [18547417.001]
  • [Cites] Br J Surg. 2010 Aug;97(8):1269-78 [20602499.001]
  • [Cites] BMJ. 2004 Sep 18;329(7467):668-73 [15374918.001]
  • [Cites] Oral Oncol. 2001 Jan;37(1):72-6 [11120486.001]
  • [Cites] J Immunol. 1984 Oct;133(4):1710-5 [6206131.001]
  • [Cites] Anticancer Res. 1998 Jan-Feb;18(1B):615-8 [9568186.001]
  • [Cites] Am Surg. 2009 Sep;75(9):754-60; discussion 761 [19774945.001]
  • [Cites] BMC Cancer. 2010 Mar 04;10:80 [20202214.001]
  • [Cites] Hepatogastroenterology. 1999 Sep-Oct;46(29):2968-73 [10576384.001]
  • [Cites] J Pathol. 2004 Jun;203(2):661-71 [15141381.001]
  • [Cites] Am J Surg. 2003 Nov;186(5):486-92 [14599612.001]
  • [Cites] Int Surg. 1991 Oct-Dec;76(4):245-9 [1663917.001]
  • [Cites] Endocr Pathol. 2008 Winter;19(4):282-8 [18931958.001]
  • [Cites] Arch Pathol Lab Med. 1998 Jan;122(1):42-6 [9448015.001]
  • [Cites] Histopathology. 1989 Aug;15(2):167-78 [2777218.001]
  • [Cites] Gut. 2007 Aug;56(8):1134-52 [17625148.001]
  • [Cites] Scand J Urol Nephrol. 1990;24(1):39-45 [2320971.001]
  • [Cites] Pancreas. 1999 Jul;19(1):26-32 [10416688.001]
  • [Cites] Anticancer Res. 2009 May;29(5):1771-6 [19443402.001]
  • [Cites] J Gastrointest Surg. 2010 Apr;14 (4):719-28 [20107918.001]
  • (PMID = 20556608.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen
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27. Farina A, Dumonceau JM, Frossard JL, Hadengue A, Hochstrasser DF, Lescuyer P: Proteomic analysis of human bile from malignant biliary stenosis induced by pancreatic cancer. J Proteome Res; 2009 Jan;8(1):159-69
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  • [Title] Proteomic analysis of human bile from malignant biliary stenosis induced by pancreatic cancer.
  • Stenosis of the common bile duct may be either due to benign (chronic pancreatitis) or malignant (cholangiocarcinoma, pancreatic adenocarcinoma) conditions.
  • To this intent, we performed a proteomic analysis of bile samples from patients having a biliary stenosis caused by pancreatic adenocarcinoma.
  • Among them, several proteins have been described as potential biomarkers of pancreatic cancer.
  • We extended our investigation by studying the expression of some of these pancreatic cancer markers in bile samples collected from patients with various etiologies of biliary stenosis including pancreatic cancer, cholangiocarcinoma, chronic pancreatitis, as well as gallstone-induced stenosis.
  • Our data showed a conspicuous overexpression of CEACAM6 and MUC1 (CA19-9) in pancreatic cancer and cholangiocarcinoma samples, according to the hypothesis that bile fluid collects cancer-associated protein leaking from the tumor microenvironment.
  • [MeSH-major] Bile / metabolism. Cholestasis / metabolism. Pancreatic Neoplasms / complications. Proteomics / methods
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, CD / biosynthesis. Biomarkers / metabolism. CA-19-9 Antigen / biosynthesis. Cell Adhesion Molecules / biosynthesis. Chromatography, Liquid / methods. Electrophoresis, Polyacrylamide Gel / methods. GPI-Linked Proteins. Humans. Mass Spectrometry / methods. Middle Aged. Mucin-1 / biosynthesis

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  • (PMID = 19055478.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / CA-19-9 Antigen; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Mucin-1
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28. Sawey ET, Johnson JA, Crawford HC: Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway. Proc Natl Acad Sci U S A; 2007 Dec 4;104(49):19327-32
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  • [Title] Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.
  • Acinar-to-ductal metaplasia in the pancreas is associated with an increased risk for tumorigenesis.
  • Molecular dissection of this process in vitro has shown that primary acinar cells, in response to EGF receptor ligands, can transdifferentiate into duct-like epithelia, passing through a nestin-positive intermediate, in a Notch pathway-dependent manner.
  • MMP-7 was found to be required for Notch activation, which leads to dedifferentiation of acinar cells to the nestin-positive transitional cell.
  • Besides being necessary for acinar transdifferentiation, it was found that MMP-7 activity was sufficient to induce the process, indicating that molecular signals capable of initiating MMP-7 expression also have the potential to induce formation of metaplastic epithelia in the pancreas.

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  • [Cites] Gastroenterology. 1999 Dec;117(6):1416-26 [10579983.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42 [17360542.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(5):1825-35 [10669757.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Int J Cancer. 2000 Oct 1;88(1):12-20 [10962434.001]
  • [Cites] Anticancer Res. 2001 Mar-Apr;21(2B):1355-8 [11396212.001]
  • [Cites] Mod Pathol. 2002 Apr;15(4):441-7 [11950919.001]
  • [Cites] J Clin Invest. 2002 Jun;109(11):1437-44 [12045257.001]
  • [Cites] Hum Mol Genet. 2002 Oct 1;11(21):2615-24 [12354787.001]
  • [Cites] Cell. 2002 Nov 27;111(5):635-46 [12464176.001]
  • [Cites] Am J Pathol. 2003 Jun;162(6):1831-43 [12759241.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5 [14657333.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1235-40 [14977820.001]
  • [Cites] Development. 2004 Sep;131(17):4213-24 [15280211.001]
  • [Cites] Cancer Res. 1985 Mar;45(3):1285-90 [2982487.001]
  • [Cites] Eur J Cell Biol. 1990 Feb;51(1):64-75 [2184038.001]
  • [Cites] Mol Carcinog. 1991;4(6):527-33 [1793490.001]
  • [Cites] Princess Takamatsu Symp. 1994;24:152-61 [8983072.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1402-7 [9037065.001]
  • [Cites] Cell. 1997 Jul 25;90(2):271-80 [9244301.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 3;89(17):1260-70 [9293916.001]
  • [Cites] Development. 1997 Oct;124(20):4133-41 [9374409.001]
  • [Cites] FEBS Lett. 1998 Sep 11;435(1):39-44 [9755855.001]
  • [Cites] Gastroenterology. 1998 Nov;115(5):1254-62 [9797382.001]
  • [Cites] Cancer Res. 1998 Dec 1;58(23):5500-6 [9850086.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):117-30 [16354684.001]
  • [Cites] Biochem J. 2006 Feb 1;393(Pt 3):679-85 [16201968.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2006 Apr;20(2):197-209 [16549324.001]
  • [Cites] J Cell Biol. 2007 Feb 12;176(4):445-58 [17296795.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] J Clin Invest. 2000 Jan;105(2):143-50 [10642592.001]
  • (PMID = 18042722.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100126; United States / NCI NIH HHS / CA / R01CA100126
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Receptors, Notch; EC 3.4.24.23 / Matrix Metalloproteinase 7
  • [Other-IDs] NLM/ PMC2148289
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29. Adachi T, Tajima Y, Kuroki T, Mishima T, Kitasato A, Tsuneoka N, Kanematsu T: Chemopreventive effects of a selective cyclooxygenase-2 inhibitor (etodolac) on chemically induced intraductal papillary carcinoma of the pancreas in hamsters. Carcinogenesis; 2008 Apr;29(4):830-3
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  • [Title] Chemopreventive effects of a selective cyclooxygenase-2 inhibitor (etodolac) on chemically induced intraductal papillary carcinoma of the pancreas in hamsters.
  • The present study was designed to determine whether etodolac, a selective cyclooxygenase-2 inhibitor, prevents chemically induced intraductal papillary carcinoma (IPC) in the main pancreatic duct of hamsters.
  • Hamsters were subjected to cholecystoduodenostomy with dissection of the distal end of the common duct.
  • The incidence of induced pancreatic carcinoma was 93, 81 and 72% in groups CE, ET and ET4, respectively.
  • The pancreatic carcinomas were histologically classified into four types, i.e. tubular, papillary, cyst adenocarcinoma and IPC.
  • The proliferating cell nuclear antigen labeling indices in the non-cancerous epithelial cells of the main pancreatic duct were 2.8 and 6.8% in groups ET4 and ET, respectively, and were significantly lower than that in group CE (10.8%).
  • Suppression of epithelial cell proliferation of the main pancreatic duct was considered as a possible mechanism of cancer prevention in this hamster model.
  • [MeSH-major] Adenocarcinoma, Papillary / drug therapy. Anticarcinogenic Agents / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase 2 Inhibitors / therapeutic use. Etodolac / therapeutic use

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  • (PMID = 18296437.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 2M36281008 / Etodolac; EC 1.14.99.1 / Cyclooxygenase 2
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30. Westgaard A, Tafjord S, Farstad IN, Cvancarova M, Eide TJ, Mathisen O, Clausen OP, Gladhaug IP: Pancreatobiliary versus intestinal histologic type of differentiation is an independent prognostic factor in resected periampullary adenocarcinoma. BMC Cancer; 2008;8:170
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  • [Title] Pancreatobiliary versus intestinal histologic type of differentiation is an independent prognostic factor in resected periampullary adenocarcinoma.
  • BACKGROUND: Resectable adenocarcinomas in the pancreatic head, by definition "periampullary", originate from ampullary, duodenal, biliary, or ductal pancreatic epithelium.
  • The aim of the study was to determine whether the histologic type of differentiation is an independent prognostic factor in periampullary adenocarcinoma, and whether tumour origin predicts the prognosis in pancreatobiliary type carcinomas independently of resection margin involvement, tumour size, nodal involvement, perineural and vascular infiltration, and degree of differentiation.
  • CONCLUSION: Pancreatobiliary versus intestinal type of differentiation independently predicts poor prognosis after pancreaticoduodenectomy for periampullary adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Ampulla of Vater / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / mortality. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Case-Control Studies. Cell Differentiation. Common Bile Duct Neoplasms / pathology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Neoplasm Invasiveness / pathology. Pancreatectomy / methods. Pancreaticoduodenectomy / methods. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome

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  • [Cites] Int J Oncol. 2000 Nov;17(5):921-6 [11029493.001]
  • [Cites] Ugeskr Laeger. 2008 Jan 28;170(5):328-30 [18252159.001]
  • [Cites] Eur J Surg Oncol. 2001 Sep;27(6):549-57 [11520088.001]
  • [Cites] Eur J Surg Oncol. 2002 Sep;28(6):637-44 [12359201.001]
  • [Cites] Am J Surg Pathol. 2004 Jul;28(7):875-82 [15223956.001]
  • [Cites] Dig Surg. 2004;21(3):202-9 [15218236.001]
  • [Cites] Am J Surg Pathol. 1989 Feb;13(2):146-62 [2644853.001]
  • [Cites] Arch Surg. 1991 Mar;126(3):353-7 [1998478.001]
  • [Cites] Jpn J Cancer Res. 1994 Feb;85(2):161-6 [7511574.001]
  • [Cites] J Natl Cancer Inst. 1994 Jun 1;86(11):829-35 [8182763.001]
  • [Cites] Br J Surg. 1995 Dec;82(12):1686-91 [8548242.001]
  • [Cites] Ann Surg. 1998 Jun;227(6):821-31 [9637545.001]
  • [Cites] Ann Surg. 1998 Jul;228(1):87-94 [9671071.001]
  • [Cites] Dig Surg. 1999;16(4):291-6 [10449973.001]
  • [Cites] Gut. 2005 Mar;54(3):385-7 [15710987.001]
  • [Cites] Ann Diagn Pathol. 2007 Feb;11(1):3-9 [17240300.001]
  • [Cites] Surg Clin North Am. 2001 Jun;81(3):543-55 [11459270.001]
  • (PMID = 18547417.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2430209
  •  go-up   go-down


31. Hruban RH, Maitra A, Kern SE, Goggins M: Precursors to pancreatic cancer. Gastroenterol Clin North Am; 2007 Dec;36(4):831-49, vi
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  • [Title] Precursors to pancreatic cancer.
  • Infiltrating ductal adenocarcinoma of the pancreas is believed to arise from morphologically distinct noninvasive precursor lesions.
  • These precursors include the intraductal papillary mucinous neoplasm, the mucinous cystic neoplasm, and pancreatic intraepithelial neoplasia.
  • Intraductal papillary mucinous neoplasms are grossly visible mucin-producing epithelial neoplasms that arise in the main pancreatic duct or one of its branches.
  • The cysts of mucinous cystic neoplasms do not communicate with the major pancreatic ducts, and these neoplasms are characterized by a distinct ovarian-type stroma.
  • Pancreatic intraepithelial neoplasia is a microscopic lesion.

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  • [Cites] J Natl Cancer Inst. 2003 Feb 5;95(3):214-21 [12569143.001]
  • [Cites] Arch Surg. 2003 Apr;138(4):427-3; discussion 433-4 [12686529.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2585-8 [12750283.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2003;10(2):147-55 [14505148.001]
  • [Cites] Mod Pathol. 2003 Oct;16(10):996-1006 [14559982.001]
  • [Cites] Mod Pathol. 2003 Nov;16(11):1086-94 [14614047.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):735-42 [14966099.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2634-8 [15059921.001]
  • [Cites] Ann Surg. 2004 Mar;239(3):400-8 [15075659.001]
  • [Cites] Pancreas. 2004 Apr;28(3):282-8 [15084972.001]
  • [Cites] Eur J Surg Oncol. 1996 Jun;22(3):232-6 [8654602.001]
  • [Cites] Am J Surg Pathol. 1996 Aug;20(8):980-94 [8712298.001]
  • [Cites] Gut. 1996 Sep;39(3):457-64 [8949654.001]
  • [Cites] Nat Genet. 1997 May;16(1):17-8 [9140390.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2140-3 [9187111.001]
  • [Cites] Gastrointest Endosc. 1998 Jan;47(1):42-9 [9468422.001]
  • [Cites] Am J Surg Pathol. 1998 Feb;22(2):163-9 [9500216.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Jun;7(6):515-21 [9641496.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4740-4 [9788631.001]
  • [Cites] Ann Diagn Pathol. 1998 Oct;2(5):286-92 [9845751.001]
  • [Cites] Am J Surg Pathol. 1999 Jan;23(1):1-16 [9888699.001]
  • [Cites] Hepatogastroenterology. 1998 Nov-Dec;45(24):2001-8 [9951854.001]
  • [Cites] Eur J Surg. 1999 Jan;165(1):43-8 [10069633.001]
  • [Cites] Am J Surg Pathol. 1999 Apr;23(4):410-22 [10199470.001]
  • [Cites] Adv Anat Pathol. 1999 Mar;6(2):65-77 [10331069.001]
  • [Cites] Am J Pathol. 1999 Jun;154(6):1835-40 [10362809.001]
  • [Cites] Ann Intern Med. 1999 Aug 17;131(4):247-55 [10454945.001]
  • [Cites] Ann Surg. 1999 Aug;230(2):152-61 [10450728.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 1999;6(3):281-5 [10526064.001]
  • [Cites] Arch Surg. 1960 Nov;81:683-9 [13738110.001]
  • [Cites] J Clin Pathol. 1962 Sep;15:432-7 [14018131.001]
  • [Cites] Nat Methods. 2004 Nov;1(2):141-7 [15782177.001]
  • [Cites] J Natl Cancer Inst. 1999 Aug 4;91(15):1310-6 [10433620.001]
  • [Cites] Mod Pathol. 2005 Jul;18(7):959-63 [15832197.001]
  • [Cites] PLoS Med. 2004 Dec;1(3):e65 [15630470.001]
  • [Cites] World J Gastroenterol. 2005 Sep 28;11(36):5688-90 [16237766.001]
  • [Cites] Am J Surg Pathol. 2006 Jan;30(1):36-41 [16330940.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Radiology. 2006 Mar;238(3):912-9 [16439566.001]
  • [Cites] Pancreatology. 2006;6(1-2):17-32 [16327281.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Jun;4(6):766-81; quiz 665 [16682259.001]
  • [Cites] Clin Cancer Res. 2006 Jun 15;12(12):3851-5 [16778113.001]
  • [Cites] Surgery. 2006 Jun;139(6):749-54 [16782429.001]
  • [Cites] Am J Surg Pathol. 2006 Sep;30(9):1067-76 [16931950.001]
  • [Cites] Ann Surg. 2006 Oct;244(4):572-82 [16998366.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Oct;4(10):1265-70 [16979953.001]
  • [Cites] Cancer Detect Prev. 2006;30(5):387-94 [17079091.001]
  • [Cites] Am J Surg Pathol. 2006 Dec;30(12):1561-9 [17122512.001]
  • [Cites] World J Surg. 2006 Dec;30(12):2236-45 [17103100.001]
  • [Cites] PLoS Med. 2006 Dec;3(12):e516 [17194196.001]
  • [Cites] J Clin Oncol. 2007 Apr 10;25(11):1417-22 [17416862.001]
  • [Cites] Ann Surg. 2004 Jun;239(6):788-97; discussion 797-9 [15166958.001]
  • [Cites] Clin Gastroenterol Hepatol. 2004 Jul;2(7):606-21 [15224285.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):977-87 [15252303.001]
  • [Cites] Cancer Res. 1976 Jul;36(7 PT 2):2690-8 [1277176.001]
  • [Cites] Am J Clin Pathol. 1978 Jun;69(6):573-80 [665578.001]
  • [Cites] Cancer. 1979 Apr;43(4):1418-28 [445339.001]
  • [Cites] Tohoku J Exp Med. 1982 Jun;137(2):115-24 [7112540.001]
  • [Cites] Virchows Arch A Pathol Anat Histol. 1982 Aug;396(3):331-49 [7135827.001]
  • [Cites] Am Surg. 1984 Apr;50(4):225-9 [6712017.001]
  • [Cites] Am J Surg Pathol. 1987 Jan;11(1):11-20 [3789255.001]
  • [Cites] Ann Surg. 1990 Oct;212(4):432-43; discussion 444-5 [2171441.001]
  • [Cites] Pathobiology. 1991;59(1):46-52 [1675057.001]
  • [Cites] Cancer. 1992 Feb 1;69(3):651-6 [1309676.001]
  • [Cites] Eur J Surg. 1995 Jan;161(1):35-40 [7727604.001]
  • [Cites] N Engl J Med. 1995 Oct 12;333(15):970-4 [7666916.001]
  • [Cites] Am J Surg Pathol. 1999 Nov;23(11):1320-7 [10555000.001]
  • [Cites] Ann Surg. 2000 Feb;231(2):205-12 [10674612.001]
  • [Cites] Am J Gastroenterol. 2000 Feb;95(2):441-5 [10685747.001]
  • [Cites] Eur J Surg. 2000 Feb;166(2):141-8 [10724492.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):2002-6 [10766191.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):1821-5 [10854204.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 2;92(15):1260-6 [10922411.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):2969-72 [10955772.001]
  • [Cites] Int J Cancer. 2000 Sep 15;87(6):809-11 [10956390.001]
  • [Cites] Am J Pathol. 2000 Sep;157(3):755-61 [10980115.001]
  • [Cites] Am J Surg Pathol. 2000 Oct;24(10):1372-7 [11023098.001]
  • [Cites] Am J Surg Pathol. 2000 Nov;24(11):1544-8 [11075857.001]
  • [Cites] Gastroenterology. 2000 Dec;119(6):1447-53 [11113065.001]
  • [Cites] AJR Am J Roentgenol. 2001 Jan;176(1):179-85 [11133563.001]
  • [Cites] Am J Surg Pathol. 2001 Jan;25(1):26-42 [11145249.001]
  • [Cites] Mod Pathol. 2001 Mar;14(3):139-46 [11266517.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] Hum Pathol. 2001 Jun;32(6):638-42 [11431719.001]
  • [Cites] Ann Surg. 2001 Sep;234(3):313-21; discussion 321-2 [11524584.001]
  • [Cites] Cancer J. 2001 Jul-Aug;7(4):251-8 [11561601.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):34-43 [11781278.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3789-93 [12097290.001]
  • [Cites] Surgery. 2002 Jul;132(1):80-5 [12110799.001]
  • [Cites] Pancreatology. 2001;1(6):648-55 [12120249.001]
  • [Cites] J Clin Gastroenterol. 2002 Aug;35(2):175-9 [12172364.001]
  • [Cites] Gastroenterology. 2002 Nov;123(5):1500-7 [12404225.001]
  • [Cites] Arch Surg. 2002 Nov;137(11):1274-8 [12413317.001]
  • [Cites] Langenbecks Arch Surg. 2002 Nov;387(7-8):281-5 [12447553.001]
  • [Cites] Virchows Arch. 2002 Nov;441(5):437-43 [12447672.001]
  • [Cites] Int J Cancer. 2003 Feb 10;103(4):525-30 [12478670.001]
  • (PMID = 17996793.001).
  • [ISSN] 0889-8553
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062924-130011; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA062924-130011
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 103
  • [Other-IDs] NLM/ NIHMS35907; NLM/ PMC2194627
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32. Parsi MA, Li A, Li CP, Goggins M: DNA methylation alterations in endoscopic retrograde cholangiopancreatography brush samples of patients with suspected pancreaticobiliary disease. Clin Gastroenterol Hepatol; 2008 Nov;6(11):1270-8
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  • BACKGROUND & AIMS: Molecular markers of pancreatic neoplasia could aid in the evaluation of suspicious pancreatic lesions where cytology is nondiagnostic.
  • We evaluated the utility of detecting and measuring aberrantly methylated DNA as markers of pancreatic and other periampullary cancers.
  • METHODS: Methylation analysis was performed on endoscopically obtained brush samples from the biliary and pancreatic ducts from 130 individuals with biliary tract strictures: 41 with pancreatic ductal adenocarcinoma, 10 with biliary tract cancers, 13 with other periampullary neoplasms, and 66 with non-neoplastic strictures including 27 with primary sclerosing cholangitis and 39 with other benign strictures.
  • RESULTS: QMSP could accurately distinguish patients with pancreatic cancer and other periampullary cancers from those with benign periampullary disease; 73.2% of patients with pancreatic ductal adenocarcinoma had at least 1 gene positive for methylation by QMSP (defined as > or =1% TFPI-2 DNA and > or =3% methylated NPTX2 and Cyclin D2 DNA) in their brush samples, compared with 80% of patients with a biliary tract cancer and only 13.6% of patients with a benign stricture (P < .001).

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  • [Cites] Cancer. 1996 Sep 1;78(5):986-90 [8780535.001]
  • [Cites] Cancer Biol Ther. 2008 Jul;7(7):1146-56 [18535405.001]
  • [Cites] Gastrointest Endosc. 1999 Mar;49(3 Pt 1):322-7 [10049415.001]
  • [Cites] Ann Intern Med. 1999 Aug 17;131(4):247-55 [10454945.001]
  • [Cites] Gut. 2004 Dec;53(12):1860-5 [15542529.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Oncogene. 2005 Jan 27;24(5):850-8 [15592528.001]
  • [Cites] Gastrointest Endosc. 2005 Mar;61(3):401-6 [15758911.001]
  • [Cites] Clin Cancer Res. 2005 Mar 15;11(6):2285-92 [15788678.001]
  • [Cites] Nat Methods. 2004 Nov;1(2):141-7 [15782177.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4681-8 [16000561.001]
  • [Cites] J Clin Oncol. 2005 Jul 10;23(20):4524-31 [16002843.001]
  • [Cites] Gastrointest Endosc. 2006 Jan;63(1):78-80 [16377320.001]
  • [Cites] Mol Cell Proteomics. 2006 Jan;5(1):157-71 [16215274.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):1208-17 [16424060.001]
  • [Cites] Gastroenterology. 2006 Feb;130(2):548-65 [16472607.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2006 Apr;20(2):211-26 [16549325.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Jun;4(6):766-81; quiz 665 [16682259.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3573-7 [11325821.001]
  • [Cites] Am J Gastroenterol. 2002 Jun;97(6):1386-91 [12094855.001]
  • [Cites] Cancer Biol Ther. 2003 Jan-Feb;2(1):78-83 [12673124.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1446-52 [12684418.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2649-57 [12750293.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3735-42 [12839967.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] Expert Rev Gastroenterol Hepatol. 2007 Oct;1(1):81-8 [19072437.001]
  • [Cites] Nucleic Acids Res. 2000 Apr 15;28(8):E32 [10734209.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1835-9 [10766168.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):871-5 [14871814.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2634-8 [15059921.001]
  • [Cites] J Am Coll Surg. 2004 May;198(5):722-31 [15110805.001]
  • [Cites] Am J Gastroenterol. 2004 May;99(5):844-50 [15128348.001]
  • [Cites] Clin Gastroenterol Hepatol. 2004 Jul;2(7):606-21 [15224285.001]
  • [Cites] Am J Gastroenterol. 2004 Aug;99(8):1464-9 [15307861.001]
  • [Cites] Am J Gastroenterol. 2004 Sep;99(9):1675-81 [15330900.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2006;13(4):286-95 [16858539.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7920-8 [16912165.001]
  • [Cites] Gastroenterology. 2006 Oct;131(4):1064-72 [17030177.001]
  • [Cites] Am J Gastroenterol. 2006 Nov;101(11):2493-500 [17029619.001]
  • [Cites] Cancer Biol Ther. 2006 Oct;5(10):1392-9 [17106238.001]
  • [Cites] Ann Surg. 2007 May;245(5):755-62 [17457168.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Jul;5(7):783-90 [17628333.001]
  • [Cites] Am J Clin Pathol. 2007 Aug;128(2):272-9 [17638662.001]
  • [Cites] Clin Cancer Res. 2007 Oct 15;13(20):6019-25 [17947463.001]
  • [Cites] Cancer Biol Ther. 2008 Jun;7(6):882-8 [18344687.001]
  • [Cites] Gastrointest Endosc. 1998 Jul;48(1):53-7 [9684665.001]
  • (PMID = 18995218.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / R01 CA120432; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA062924-130008; United States / NCI NIH HHS / CA / R01 CA120432-03; United States / NCI NIH HHS / CA / CA120432-03; United States / NCI NIH HHS / CA / P50 CA062924-130008
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Glycoproteins; 0 / Nerve Tissue Proteins; 0 / neuronal pentraxin; 0 / tissue-factor-pathway inhibitor 2; 9007-41-4 / C-Reactive Protein
  • [Other-IDs] NLM/ NIHMS85843; NLM/ PMC2636968
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33. Oshiro H, Matsuo K, Mawatari H, Inayama Y, Yamanaka S, Nagahama K, Endo I, Shimada H, Nakajima A, Kubota K: Mucin-producing gallbladder adenocarcinoma with focal small cell and large cell neuroendocrine differentiation associated with pancreaticobiliary maljunction. Pathol Int; 2008 Dec;58(12):780-6
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  • [Title] Mucin-producing gallbladder adenocarcinoma with focal small cell and large cell neuroendocrine differentiation associated with pancreaticobiliary maljunction.
  • Although the patient's status and laboratory data initially suggested biliary pancreatitis due to gallstone, radiography and endoscopy confirmed the presence of pancreaticobiliary maljunction and a gallbladder tumor with excessive mucin, in which the duodenal papilla and the common bile duct were impacted.
  • Additionally, small foci of small cell and large cell neuroendocrine carcinomatous components were observed.
  • Thus, the final classification of pT2N0M0 stage II was given to this lesion, according to the Union Internationale Contre le Cancer guidelines.
  • [MeSH-major] Adenocarcinoma / pathology. Common Bile Duct / abnormalities. Gallbladder Neoplasms / pathology. Mucins / metabolism. Pancreatic Ducts / abnormalities

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  • (PMID = 19067853.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
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34. Satoh K, Hamada S, Kanno A, Hirota M, Umino J, Ito H, Masamune A, Egawa S, Unno M, Shimosegawa T: Expression of MSX2 predicts malignancy of branch duct intraductal papillary mucinous neoplasm of the pancreas. J Gastroenterol; 2010 Jul;45(7):763-70
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  • [Title] Expression of MSX2 predicts malignancy of branch duct intraductal papillary mucinous neoplasm of the pancreas.
  • BACKGROUND: To distinguish malignant from benign branch duct (BD)-intraductal papillary mucinous neoplasm (IPMN) still remains difficult.
  • Recently, we revealed that MSX2 was frequently expressed in pancreatic cancer and its expression was correlated with aggressive behavior of the cancer.
  • The role of MSX2 in the pancreatic duct cell was assessed by the induced expression of MSX2 in a normal human pancreatic duct epithelial cell line (HPDE).
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Papillary / genetics. Homeodomain Proteins / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / pathology. Aged. Cell Line. Cell Proliferation. Epithelial Cells / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Multivariate Analysis. Pancreatic Ducts / cytology. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology. Predictive Value of Tests. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] J Comput Assist Tomogr. 2004 Jan-Feb;28(1):117-22 [14716244.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4222-6 [9766641.001]
  • [Cites] Int J Cancer. 2006 May 1;118(9):2269-75 [16331618.001]
  • [Cites] Dev Biol. 1999 Jan 15;205(2):260-74 [9917362.001]
  • [Cites] Oncol Rep. 2008 May;19(5):1185-90 [18425375.001]
  • [Cites] Am J Pathol. 2008 Apr;172(4):926-39 [18349132.001]
  • [Cites] Gastrointest Endosc. 1998 Aug;48(2):164-71 [9717782.001]
  • [Cites] Oncogene. 2001 Apr 19;20(17):2153-60 [11360199.001]
  • [Cites] J Gastrointest Surg. 2002 Sep-Oct;6(5):662-3 [12399053.001]
  • [Cites] Br J Surg. 2003 Oct;90(10):1244-9 [14515294.001]
  • [Cites] Hepatogastroenterology. 1998 Nov-Dec;45(24):2009-15 [9951855.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7482-6 [1977161.001]
  • [Cites] Arch Surg. 1999 Oct;134(10 ):1131-6 [10522860.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2004 Apr;9(2):195-205 [15300013.001]
  • [Cites] Pancreas. 1996 May;12(4):362-8 [8740403.001]
  • [Cites] Development. 1996 Sep;122(9):2729-37 [8787747.001]
  • [Cites] J Gastrointest Surg. 2003 Jan;7(1):12-8; discussion 18-9 [12559180.001]
  • [Cites] J Cell Physiol. 2007 Dec;213(3):768-74 [17516553.001]
  • [Cites] Arch Surg. 2002 Nov;137(11):1274-8 [12413317.001]
  • [Cites] Dev Biol. 1999 May 15;209(2):298-307 [10328922.001]
  • [Cites] Nature. 1991 Aug 1;352(6334):429-31 [1677742.001]
  • [Cites] Surgery. 2002 Jul;132(1):80-5 [12110799.001]
  • [Cites] J Clin Gastroenterol. 2003 Mar;36(3):261-5 [12590239.001]
  • [Cites] Int J Pancreatol. 1993 Oct;14(2):135-43 [8283077.001]
  • [Cites] Cancer. 2001 Jul 15;92(2):271-8 [11466679.001]
  • [Cites] Gastroenterology. 1996 Jun;110(6):1909-18 [8964418.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Sep;20(9):1379-84 [16105124.001]
  • [Cites] Oncogene. 2007 Nov 29;26(54):7526-34 [17546050.001]
  • [Cites] Am J Surg Pathol. 2000 Oct;24(10):1372-7 [11023098.001]
  • [Cites] Am J Gastroenterol. 2007 Aug;102(8):1759-64 [17686073.001]
  • [Cites] J Pathol. 2006 Sep;210(1):42-8 [16794990.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):51-6 [8099533.001]
  • [Cites] Am J Pathol. 2001 Feb;158(2):419-29 [11159180.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Jul 15;194(1):187-93 [7687426.001]
  • [Cites] Mod Pathol. 2007 Dec;20(12):1238-44 [17906614.001]
  • [Cites] J Gastroenterol Hepatol. 2003 Nov;18(11):1323-4 [14535994.001]
  • [Cites] Nihon Shokakibyo Gakkai Zasshi. 2007 Sep;104(9):1338-43 [17827904.001]
  • [Cites] Am J Pathol. 1996 Jun;148(6):1763-70 [8669463.001]
  • [Cites] J Gastroenterol. 2005 Jul;40(7):744-51 [16082592.001]
  • [Cites] Gut. 2002 Jun;50(6):861-8 [12010891.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):34-43 [11781278.001]
  • [Cites] Development. 1993 Feb;117(2):461-70 [8101167.001]
  • [Cites] Oncogene. 1996 May 16;12(10):2137-46 [8668339.001]
  • (PMID = 20107842.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MSX2 protein; 0 / RNA, Messenger
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35. Iwamuro M, Kubota J, Saito S, Goubaru M, Ohta T, Ogata M, Takuma Y, Tanaka S, Makino Y, Murakami I: [A case of mixed duct-islet cell tumor of the pancreas]. Nihon Shokakibyo Gakkai Zasshi; 2007 Jun;104(6):829-36
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  • [Title] [A case of mixed duct-islet cell tumor of the pancreas].
  • The tumor on the pancreatic body of 22 mm size was revealed by close inspection, and was diagnosed as insulinoma.
  • Surgical resection was performed, but curative resection was impossible because the component of adenocarcinoma infiltrating into surrounding tissue coexisted with insulinoma.
  • Postoperatively, we make a diagnosis of combined tumor of the pancreas, i.e. mixed duct-islet cell carcinoma.
  • [MeSH-major] Carcinoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Insulinoma / diagnosis. Neoplasms, Multiple Primary. Pancreatic Neoplasms / diagnosis

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  • (PMID = 17548951.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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36. Salla C, Chatzipantelis P, Konstantinou P, Karoumpalis I, Sakellariou S, Pantazopoulou A, Manika Z: Endoscopic ultrasound-guided fine-needle aspiration cytology in the diagnosis of intraductal papillary mucinous neoplasms of the pancreas. A study of 8 cases. JOP; 2007;8(6):715-24
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  • [Title] Endoscopic ultrasound-guided fine-needle aspiration cytology in the diagnosis of intraductal papillary mucinous neoplasms of the pancreas. A study of 8 cases.
  • CONTEXT: Intraductal papillary mucinous neoplasm (IPMN) is an increasingly recognized neoplasm of the pancreas, accounting for 5% of pancreatic neoplasms, it is considered difficult to diagnose by fine-needle aspiration (FNA) cytology.
  • OBJECTIVE: The aim of this study was to investigate the role of EUS-guided FNA cytology in the diagnosis of IPMN of the pancreas.
  • EUS/clinical findings, macroscopic/microscopic features of cell blocks and smears, and immunocytochemical stains accompanied by histopathologic diagnosis were recorded and studied.
  • RESULTS: EUS revealed hypoechoic masses in the head of pancreas (n=6) and in the body/tail (n=2), measuring from 16.6 to 35.8 mm.
  • In all cases, the hypoechoic mass had a distinctive distribution, involving the main pancreatic duct and/or the associated large branch ducts while intraductal nodules or multiple cysts were detected.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Papillary / diagnosis. Adenocarcinoma, Papillary / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology


37. Al-Wadei HA, Al-Wadei MH, Schuller HM: Prevention of pancreatic cancer by the beta-blocker propranolol. Anticancer Drugs; 2009 Jul;20(6):477-82
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  • [Title] Prevention of pancreatic cancer by the beta-blocker propranolol.
  • Pancreatic ductal adenocarcinoma (PDAC) is among the leading causes of cancer deaths and is unresponsive to existing therapy.
  • We found that propranolol had strong cancer preventive effects in this animal model.
  • Western blots of pancreatic duct cells and PDAC cells harvested by laser capture microscopy showed significant upregulation of the alpha7 nAChR associated with significant inductions of p-CREB, p-ERK1/2, and increases in epidermal growth factor and vascular endothelial growth factor in PDAC cells of hamsters not treated with propranolol.
  • [MeSH-major] Adrenergic beta-Antagonists / therapeutic use. Anticarcinogenic Agents / therapeutic use. Carcinoma, Pancreatic Ductal / prevention & control. Pancreatic Neoplasms / prevention & control. Propranolol / therapeutic use. Receptors, Adrenergic, beta / metabolism

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  • [Cites] Mol Pharmacol. 2006 Feb;69(2):618-28 [16269536.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):369-75 [16428474.001]
  • [Cites] Int J Cancer. 2006 Jun 1;118(11):2744-9 [16381019.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Jun;58(3):231-41 [16725343.001]
  • [Cites] Cancer Biol Ther. 2006 May;5(5):511-7 [16582591.001]
  • [Cites] Int J Cancer. 2006 Oct 1;119(7):1547-52 [16671086.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10357-64 [17079456.001]
  • [Cites] Toxicol Sci. 2007 Mar;96(1):21-9 [17003101.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1164-73 [17315157.001]
  • [Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S113-31 [17486047.001]
  • [Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S61-70 [17486053.001]
  • [Cites] Toxicol Sci. 2007 Jun;97(2):279-87 [17369603.001]
  • [Cites] Life Sci. 2007 May 30;80(24-25):2274-80 [17459420.001]
  • [Cites] Toxicol Appl Pharmacol. 2007 Jun 15;221(3):261-7 [17498763.001]
  • [Cites] J Cell Biochem. 2005 Jul 1;95(4):649-56 [15849724.001]
  • [Cites] Cancer. 2007 Aug 15;110(4):738-44 [17580363.001]
  • [Cites] Eur J Cancer. 2009 May;45(7):1257-64 [19254833.001]
  • [Cites] Nat Rev Cancer. 2009 Mar;9(3):195-205 [19194381.001]
  • [Cites] Anticancer Drugs. 2008 Aug;19(7):655-71 [18594207.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1737-44 [17557921.001]
  • [Cites] Carcinogenesis. 2001 Mar;22(3):473-9 [11238189.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2866-9 [11306460.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Oct;128(10):525-32 [12384795.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jul;80(1):63-70 [12889599.001]
  • [Cites] Ann N Y Acad Sci. 2003 Sep;998:66-80 [14592864.001]
  • [Cites] J Biol Chem. 2004 Sep 17;279(38):40209-19 [15210690.001]
  • [Cites] Cancer Res. 1993 Jun 1;53(11):2498-501 [8495411.001]
  • [Cites] Prog Brain Res. 1996;109:125-37 [9009699.001]
  • [Cites] Cardiovasc Drugs Ther. 1997 Jan;10(6):657-65 [9110108.001]
  • [Cites] Endocrinology. 1997 Jun;138(6):2601-9 [9165054.001]
  • [Cites] Biochem Pharmacol. 1998 May 1;55(9):1377-84 [10076528.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4510-5 [10493497.001]
  • [Cites] Alcohol Clin Exp Res. 2007 Sep;31(9):1467-72 [17760784.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5272-7 [15958573.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Oct;131(10):639-48 [16091975.001]
  • (PMID = 19387337.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829; United States / NCI NIH HHS / CA / R01 CA042829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic beta-Antagonists; 0 / Anticarcinogenic Agents; 0 / Chrna7 protein, human; 0 / Nitrosamines; 0 / Receptors, Adrenergic, beta; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 3K9958V90M / Ethanol; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 9Y8NXQ24VQ / Propranolol; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ NIHMS380612; NLM/ PMC3366433
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38. Novak I, Hede SE, Hansen MR: Adenosine receptors in rat and human pancreatic ducts stimulate chloride transport. Pflugers Arch; 2008 May;456(2):437-47
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  • [Title] Adenosine receptors in rat and human pancreatic ducts stimulate chloride transport.
  • Previously, we have shown that pancreatic acini release adenosine triphosphate (ATP) and ATP-handling enzymes, and pancreatic ducts express various purinergic P2 receptors.
  • The aim of the present study was to establish whether pancreatic ducts also express adenosine receptors and whether these could be involved in secretory processes, which involve cystic fibrosis transmembrane regulator (CFTR) Cl- channels or Ca2+-activated Cl- channels and H(+)/HCO(-)(3) transporters.
  • Reverse transcriptase polymerase chain reaction analysis on rat pancreatic ducts and human duct cell adenocarcinoma lines showed that they express A1, A2A, A2B, and A3 receptors.
  • Real-time PCR revealed relatively low messenger RNA levels of adenosine receptors compared to beta-actin; the rank order for the receptors was A2A>A2B>or=A3>>A1 for rat pancreas and A2B>A2A>>A3>or=A1 for duct cell lines.
  • Whole-cell patch-clamp recordings on rat pancreatic ducts showed that, in about half of the recordings, adenosine depolarized the membrane voltage, and this was because of the opening of Cl- channels.
  • Using a Cl--sensitive fluorophore and single-cell imaging on duct cell lines, it was found that 58% of PANC-1 cells responded to adenosine, whereas only 9% of CFPAC-1 cells responded.
  • Adenosine elicited Ca2+ signals only in a few rat and human duct cells, which did not seem to correlate with Cl- signals.
  • A2A receptors were localized in the luminal membranes of rat pancreatic ducts, plasma membrane of many PANC-1 cells, but only a few CFPAC-1 cells.
  • Taken together, our data indicate that A2A receptors open Cl- channels in pancreatic ducts cells with functional CFTR.
  • We propose that adenosine can stimulate pancreatic secretion and, thereby, is an active player in the acini-to-duct signaling.
  • [MeSH-major] Chloride Channels / metabolism. Pancreatic Ducts / metabolism. Receptors, Purinergic P1 / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Calcium Signaling / physiology. Cell Line, Tumor. Chlorides / metabolism. Cystic Fibrosis Transmembrane Conductance Regulator / genetics. Cystic Fibrosis Transmembrane Conductance Regulator / metabolism. Epithelial Cells / cytology. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. Humans. Male. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Patch-Clamp Techniques. Rats. Rats, Wistar. Receptors, Adenosine A2 / genetics. Receptors, Adenosine A2 / metabolism

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  • [Cites] Rocz Akad Med Bialymst. 2003;48:57-60 [14737942.001]
  • [Cites] Am J Physiol. 1999 Aug;277(2 Pt 1):C205-15 [10444396.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jun 15;89(12 ):5562-6 [1376923.001]
  • [Cites] Anal Biochem. 1996 Oct 1;241(1):51-8 [8921165.001]
  • [Cites] Eur J Pharmacol. 1985 Dec 3;118(3):203-9 [4085553.001]
  • [Cites] Cardiovasc Res. 2004 Sep 1;63(4):739-46 [15306230.001]
  • [Cites] J Clin Invest. 1993 Mar;91(3):1253-7 [7680666.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 May;288(5):G972-7 [15637180.001]
  • [Cites] Gastroenterology. 2000 Sep;119(3):829-36 [10982777.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):14120-5 [11707576.001]
  • [Cites] FASEB J. 2000 Nov;14(14):2345-56 [11053257.001]
  • [Cites] Life Sci. 1995;57(17):PL253-8 [7564900.001]
  • [Cites] J Biol Chem. 1995 Feb 3;270(5):2387-94 [7836474.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Nov;287(5):G1100-7 [15256361.001]
  • [Cites] J Biol Chem. 2001 Aug 31;276(35):32925-32 [11387334.001]
  • [Cites] J Biol Chem. 2006 Oct 6;281(40):29441-7 [16885159.001]
  • [Cites] Am J Physiol. 1996 Aug;271(2 Pt 1):C469-77 [8769985.001]
  • [Cites] Clin Exp Pharmacol Physiol. 1986 May;13(5):425-32 [3742885.001]
  • [Cites] J Membr Biol. 1988 Oct;105(2):131-42 [2464063.001]
  • [Cites] Br J Pharmacol. 2006 Sep;149(1):43-55 [16880767.001]
  • [Cites] Nat Rev Drug Discov. 2006 Mar;5(3):247-64 [16518376.001]
  • [Cites] J Physiol. 2004 Mar 1;555(Pt 2):311-21 [14694149.001]
  • [Cites] Pflugers Arch. 1988 May;411(5):546-53 [2455270.001]
  • [Cites] Am J Physiol. 1996 Nov;271(5 Pt 1):G747-54 [8944687.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Jun;280(6):C1387-93 [11350733.001]
  • [Cites] J Biol Chem. 1995 Jun 23;270(25):15175-80 [7797501.001]
  • [Cites] Cell Physiol Biochem. 2002;12(2-3):83-92 [12077553.001]
  • [Cites] Br J Pharmacol. 1998 Aug;124(8):1597-606 [9756374.001]
  • [Cites] Pharmacol Rev. 2001 Dec;53(4):527-52 [11734617.001]
  • [Cites] News Physiol Sci. 2003 Feb;18:12-7 [12531926.001]
  • [Cites] Eur J Pharmacol. 2002 Nov 1;454(1):85-93 [12409009.001]
  • [Cites] Fundam Clin Pharmacol. 2000 May-Jun;14(3):203-8 [15602796.001]
  • [Cites] Annu Rev Physiol. 2005;67:377-409 [15709963.001]
  • [Cites] J Physiol. 2006 Oct 1;576(Pt 1):163-78 [16857709.001]
  • [Cites] J Biol Chem. 1999 Nov 5;274(45):31784-91 [10542200.001]
  • [Cites] Pflugers Arch. 1998 Jun;436(1):33-9 [9560444.001]
  • [Cites] Pancreas. 2002 Jan;24(1):75-82 [11741185.001]
  • [Cites] Am J Physiol. 1999 Feb;276(2 Pt 1):C361-9 [9950763.001]
  • [Cites] Biochemistry. 1995 Jul 18;34(28):9088-94 [7542477.001]
  • [Cites] Biochemistry. 1997 May 27;36(21):6455-61 [9174362.001]
  • [Cites] J Membr Biol. 1990 Feb;113(3):193-202 [2335807.001]
  • (PMID = 18057956.001).
  • [ISSN] 0031-6768
  • [Journal-full-title] Pflugers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chloride Channels; 0 / Chlorides; 0 / Receptors, Adenosine A2; 0 / Receptors, Purinergic P1; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator
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39. Neupane D, Korc M: 14-3-3sigma Modulates pancreatic cancer cell survival and invasiveness. Clin Cancer Res; 2008 Dec 1;14(23):7614-23
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  • [Title] 14-3-3sigma Modulates pancreatic cancer cell survival and invasiveness.
  • PURPOSE: The purpose of the present study was to investigate the potential role of 14-3-3sigma in pancreatic ductal adenocarcinoma (PDAC).
  • EXPERIMENTAL DESIGN: 14-3-3 isoform expression was determined by real-time quantitative PCR in laser capture normal pancreatic ductal cells and pancreatic cancer cells and in 5 pancreatic cancer cell lines.
  • RESULTS: The cancer cells in 7 PDAC samples expressed high levels of 14-3-3sigma mRNA by quantitative PCR when compared with normal pancreatic duct cells.
  • Most cell lines released detectable amount of 14-3-3sigma into conditioned medium.
  • CONCLUSIONS: 14-3-3sigma contributes to the chemoresistance of pancreatic cancer cells and exerts cell type-dependent effects on cell migration and invasion.

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  • [Cites] Electrophoresis. 1999 Oct;20(14):2952-60 [10546833.001]
  • [Cites] Laryngoscope. 2000 Mar;110(3 Pt 1):374-81 [10718422.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 May 23;97(11):6049-54 [10811911.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2000;40:617-47 [10836149.001]
  • [Cites] Oncogene. 2000 Nov 2;19(46):5298-302 [11077447.001]
  • [Cites] Front Biosci. 2001 May 1;6:D685-707 [11333208.001]
  • [Cites] Anticancer Res. 2001 May-Jun;21(3B):1919-24 [11497278.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2931-40 [11555612.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45201-6 [11574543.001]
  • [Cites] Nature. 2002 Jun 20;417(6891):871-5 [12075357.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):897-909 [12459728.001]
  • [Cites] Mol Cancer Ther. 2002 Jan;1(3):161-7 [12467210.001]
  • [Cites] J Biol Chem. 2003 Jan 17;278(3):2058-65 [12426317.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2649-57 [12750293.001]
  • [Cites] Cell Mol Life Sci. 2003 Jun;60(6):1180-99 [12861384.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4158-66 [12874021.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14):5127-36 [14613990.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):931-43 [14737123.001]
  • [Cites] Oncogene. 2004 Mar 25;23(13):2385-400 [14767473.001]
  • [Cites] Biochem J. 2004 Apr 15;379(Pt 2):395-408 [14744259.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):3064-8 [15131044.001]
  • [Cites] J Invest Dermatol. 2004 May;122(5):1188-97 [15140222.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3599-606 [15150118.001]
  • [Cites] Int J Oncol. 2004 Jul;25(1):203-10 [15202007.001]
  • [Cites] Mol Cancer. 2003 Jan 7;2:6 [12605713.001]
  • [Cites] Mol Cancer. 2003 Jan 22;2:14 [12605717.001]
  • [Cites] Carcinogenesis. 2004 Sep;25(9):1575-85 [15073049.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] J Biol Chem. 1990 Jun 25;265(18):10466-72 [2141333.001]
  • [Cites] Growth Factors. 1993;8(1):23-34 [8383514.001]
  • [Cites] N Engl J Med. 2008 Mar 13;358(11):1160-74 [18337605.001]
  • [Cites] Anticancer Res. 1993 May-Jun;13(3):565-9 [8317885.001]
  • [Cites] Cell. 1996 Mar 22;84(6):889-97 [8601312.001]
  • [Cites] Cell. 1996 Nov 15;87(4):619-28 [8929531.001]
  • [Cites] Surg Oncol Clin N Am. 1998 Jan;7(1):25-41 [9443985.001]
  • [Cites] J Biol Chem. 1998 Mar 27;273(13):7495-500 [9516449.001]
  • [Cites] Mol Cell. 1997 Dec;1(1):3-11 [9659898.001]
  • [Cites] Nature. 1999 Oct 7;401(6753):616-20 [10524633.001]
  • [Cites] Oncogene. 2004 Dec 2;23(56):9034-41 [15489902.001]
  • [Cites] J Invest Dermatol. 2005 Jan;124(1):170-7 [15654971.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3274-9 [15867223.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):18891-8 [15731107.001]
  • [Cites] Pancreas. 2005 Oct;31(3):263-74 [16163059.001]
  • [Cites] Clin Exp Metastasis. 2005;22(6):461-73 [16320109.001]
  • [Cites] Am J Pathol. 2006 Mar;168(3):962-72 [16507911.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3248-55 [16540677.001]
  • [Cites] J Clin Invest. 2008 Jan;118(1):89-99 [18064304.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • (PMID = 19047086.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075059; United States / NCI NIH HHS / CA / CA-10130; United States / NCI NIH HHS / CA / CA101306-05; United States / NCI NIH HHS / CA / R01 CA101306; United States / NCI NIH HHS / CA / R01 CA101306-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14-3-3 Proteins
  • [Other-IDs] NLM/ NIHMS85737; NLM/ PMC3142357
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40. Li M, Bharadwaj U, Zhang R, Zhang S, Mu H, Fisher WE, Brunicardi FC, Chen C, Yao Q: Mesothelin is a malignant factor and therapeutic vaccine target for pancreatic cancer. Mol Cancer Ther; 2008 Feb;7(2):286-96
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  • [Title] Mesothelin is a malignant factor and therapeutic vaccine target for pancreatic cancer.
  • Given the high fatality rate of pancreatic cancer, an effective treatment for this devastating disease is urgently needed.
  • We have shown that mesothelin expression was higher in human pancreatic cancer cells than in human pancreatic duct epithelial cells, and mesothelin mRNA was substantially overexpressed in 18 of 21 (86%) clinical pancreatic adenocarcinoma specimens when compared with the surrounding normal tissues.
  • Here we studied the effects of mesothelin overexpression in pancreatic cancer cell proliferation and migration in vitro and pancreatic cancer progression in vivo.
  • We found that forced expression of mesothelin significantly increased tumor cell proliferation and migration by 90% and 300%, respectively, and increased tumor volume by 4-fold in the nude mice xenograft model when compared with the vector control cell line.
  • Silencing of mesothelin inhibited cell proliferation and migration in pancreatic cancer cells and ablated tumor progression in vivo.
  • This study revealed novel functions of mesothelin and suggested a new therapeutic vaccine strategy whereby mesothelin is targeted to control pancreatic cancer progression.

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  • [Cites] J Immunol. 2002 Dec 1;169(11):6120-6 [12444114.001]
  • [Cites] Am J Clin Pathol. 2002 May;117(5):755-65 [12090425.001]
  • [Cites] Hum Pathol. 2003 Jun;34(6):605-9 [12827615.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4158-66 [12874021.001]
  • [Cites] Expert Rev Vaccines. 2002 Jun;1(1):101-9 [12908517.001]
  • [Cites] Virology. 2003 Sep 1;313(2):502-13 [12954217.001]
  • [Cites] Mod Pathol. 2003 Sep;16(9):902-12 [13679454.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):9190-8 [14676194.001]
  • [Cites] Lancet. 2004 Mar 27;363(9414):1049-57 [15051286.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):3987-93 [15173012.001]
  • [Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):3937-42 [15217923.001]
  • [Cites] J Immunol. 2004 Aug 1;173(3):1951-8 [15265929.001]
  • [Cites] Cancer Res. 1984 Feb;44(2):717-26 [6692374.001]
  • [Cites] Cancer Res. 1992 Jan 1;52(1):181-6 [1727378.001]
  • [Cites] Am J Pathol. 1993 Aug;143(2):545-54 [8342602.001]
  • [Cites] Am J Pathol. 1994 May;144(5):889-95 [8178941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):136-40 [8552591.001]
  • [Cites] Hum Pathol. 1996 Feb;27(2):119-24 [8617452.001]
  • [Cites] Am J Pathol. 1996 Jun;148(6):1763-70 [8669463.001]
  • [Cites] CA Cancer J Clin. 1998 Jan-Feb;48(1):6-29 [9449931.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):109-12 [9488584.001]
  • [Cites] J Pathol. 1998 Nov;186(3):247-53 [10211112.001]
  • [Cites] Cancer. 2004 Nov 15;101(10):2341-50 [15476280.001]
  • [Cites] Vaccine. 2004 Nov 25;23(2):139-47 [15531030.001]
  • [Cites] J Virol. 2005 Jan;79(2):717-24 [15613299.001]
  • [Cites] Am J Surg Pathol. 2005 Mar;29(3):381-9 [15725808.001]
  • [Cites] Pancreas. 2005 May;30(4):349-54 [15841046.001]
  • [Cites] Nat Rev Cancer. 2005 Jun;5(6):459-67 [15905855.001]
  • [Cites] Clin Cancer Res. 2005 Aug 1;11(15):5356-64 [16061848.001]
  • [Cites] Immunol Res. 2005;32(1-3):155-68 [16106066.001]
  • [Cites] Clin Cancer Res. 2005 Sep 1;11(17):6342-51 [16144939.001]
  • [Cites] Int J Gynecol Cancer. 2005 Nov-Dec;15 Suppl 3:274-81 [16343244.001]
  • [Cites] Am J Clin Pathol. 2005 Dec;124(6):838-45 [16416732.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):898-906 [16424023.001]
  • [Cites] Eur J Immunol. 2006 May;36(5):1337-49 [16619291.001]
  • [Cites] Cancer. 2006 May 15;106(10):2284-94 [16604531.001]
  • [Cites] Mol Cancer. 2006;5(1):50 [17067392.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1571-5 [17332303.001]
  • [Cites] Gynecol Oncol. 2007 Jun;105(3):563-70 [17400285.001]
  • [Cites] Eur J Haematol. 2007 Oct;79(4):281-6 [17803679.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Nov 20;104(47):18636-41 [18003899.001]
  • [Cites] Nat Med. 2000 Oct;6(10):1160-6 [11017149.001]
  • [Cites] J Clin Oncol. 2001 Jan 1;19(1):145-56 [11134207.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476.001]
  • [Cites] Mod Pathol. 2003 Mar;16(3):192-7 [12640097.001]
  • (PMID = 18281514.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / R21 AT003094-01; United States / NIDCR NIH HHS / DE / DE15542; United States / NIDCR NIH HHS / DE / DE015543-02; United States / NIDCR NIH HHS / DE / R01 DE015543; United States / NIDCR NIH HHS / DE / R01 DE015543-02; United States / NCCIH NIH HHS / AT / AT003094; United States / NCCIH NIH HHS / AT / R21 AT003094; United States / NCCIH NIH HHS / AT / AT003094-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 0 / mesothelin
  • [Other-IDs] NLM/ NIHMS228173; NLM/ PMC2929838
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41. Geismann C, Morscheck M, Koch D, Bergmann F, Ungefroren H, Arlt A, Tsao MS, Bachem MG, Altevogt P, Sipos B, Fölsch UR, Schäfer H, Müerköster SS: Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer. Cancer Res; 2009 May 15;69(10):4517-26
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  • [Title] Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer.
  • Pancreatic ductal adenocarcinoma (PDAC) is thought to originate from ductal structures, exhibiting strong desmoplastic reaction with stromal pancreatic myofibroblasts (PMF), which are supposed to drive PDAC tumorigenesis.
  • Thus, this study aimed to investigate whether PMFs are involved in the induction of tumoral L1CAM and whether this contributes to malignant transformation of pancreatic ductal cells and PDAC tumorigenesis.
  • Immunohistochemistry of tissues from chronic pancreatitis specimens revealed considerable L1CAM expression in ductal structures surrounded by dense fibrotic tissue, whereas no L1CAM staining was seen in normal pancreatic tissues.
  • Using the human pancreatic duct cell line H6c7, we show that coculture with PMFs led to a transforming growth factor-beta1 (TGF-beta1)-dependent up-regulation of L1CAM expression.
  • This mechanism of TGF-beta1-induced L1CAM expression and the resulting phenotype could be verified in the TGF-beta1-responsive PDAC cell lines Colo357 and Panc1.
  • Our data provide new insights into the mechanisms of tumoral L1CAM induction and how PMFs contribute to malignant transformation of pancreatic duct cells early in PDAC tumorigenesis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Neural Cell Adhesion Molecule L1 / genetics. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Transcription Factors / physiology. Transforming Growth Factor beta1 / physiology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. Cell Line. Cell Line, Tumor. Cell Movement. Cell Transformation, Neoplastic. Coculture Techniques. Humans. Mice. Pancreatitis / pathology. Pancreatitis / surgery. RNA, Small Interfering / genetics. Transfection. Up-Regulation

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  • (PMID = 19435915.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecule L1; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / snail family transcription factors
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42. Pimenova EL, Bogatyrev VN, Chistiakova OV: [Evaluation of the diagnostic significance of cytologic studies in pancreatic tumors]. Klin Lab Diagn; 2006 Apr;(4):32-6
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  • [Title] [Evaluation of the diagnostic significance of cytologic studies in pancreatic tumors].
  • The study was undertaken to specify cytomorphological criteria for prostatic duct adenocarcinoma (PDAC), by assessing fine-needle aspiration biopsy (FNAB) specimens.
  • For statistical analysis, the authors selected the following cytological signs of malignancy: anisonucleosis, increased nuclei, hyperchromia, uneven chromatin distribution, enucleation, uneven nuclear outline, apocytes; increased nucleoli, nucleolar polymorphism, multiple nucleoli, increased cells, anisocytosis (polymorphism of the size and shape of a cell, mitoses, piled nuclei, papillary structures, slightly glandular structures.
  • [MeSH-major] Adenocarcinoma / diagnosis. Pancreatic Ducts / pathology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 16756163.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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43. Martínez-Romero C, Rooman I, Skoudy A, Guerra C, Molero X, González A, Iglesias M, Lobato T, Bosch A, Barbacid M, Real FX, Hernández-Muñoz I: The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma. J Pathol; 2009 Oct;219(2):205-13
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  • [Title] The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma.
  • Chronic pancreatitis and pancreatic ductal adenocarcinoma (PDAC) are associated with major changes in cell differentiation.
  • Polycomb proteins are epigenetic silencers expressed in adult stem cells; up-regulation of Polycomb proteins has been reported to occur in a variety of solid tumours such as colon and breast cancer.
  • We hypothesized that Polycomb might play a role in preneoplastic states in the pancreas and in tumour development/progression.
  • To test these ideas, we determined the expression of PRC1 complex proteins (Bmi1 and Ring1b) during pancreatic development and in pancreatic tissue from mouse models of disease: acute and chronic pancreatic injury, duct ligation, and in K-Ras(G12V) conditional knock-in and caerulein-treated K-Ras(G12V) mice.
  • The study was extended to human pancreatic tissue samples.
  • To obtain mechanistic insights, Bmi1 expression in cells undergoing in vitro exocrine cell metaplasia and the effects of Bmi1 depletion in an acinar cancer cell line were studied.
  • We found that Bmi1 and Ring1B are expressed in pancreatic exocrine precursor cells during early development and in ductal and islet cells-but not acinar cells-in the adult pancreas.
  • Bmi1 expression was induced in acinar cells during acute injury, in acinar-ductal metaplastic lesions, as well as in pancreatic intraepithelial neoplasia (PanIN) and PDAC.
  • Our results suggest that Bmi1 and Ring1B are modulated in pancreatic diseases and could contribute differently to tumour development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Nuclear Proteins / metabolism. Pancreatic Neoplasms / metabolism. Pancreatitis, Chronic / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cells, Cultured. Disease Models, Animal. Humans. Male. Metaplasia / metabolism. Mice. Mice, Inbred C57BL. Pancreas / metabolism. Pancreas, Exocrine / metabolism. Pancreas, Exocrine / pathology. Pancreatitis / metabolism. Polycomb Repressive Complex 1. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Wistar. Transcription Factors / metabolism

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  • [Copyright] 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 19585519.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Bmi1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / transcription factor PTF1; EC 6.3.2.19 / Polycomb Repressive Complex 1
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44. Pryczynicz A, Guzińska-Ustymowicz K, Kemona A, Czyzewska J: Expression of the E-cadherin-catenin complex in patients with pancreatic ductal adenocarcinoma. Folia Histochem Cytobiol; 2010 Jan 1;48(1):128-33
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  • [Title] Expression of the E-cadherin-catenin complex in patients with pancreatic ductal adenocarcinoma.
  • Changes in their expression and functioning reflect invasive and metastatic properties of cancer cells.
  • The study objective was to assess changes in the expressions of E-cadherin and alpha-, beta- and gamma-catenin proteins in pancreatic duct carcinoma in correlation with clinicopathological parameters, lymph node involvement and distant metastases.
  • Twenty-nine patients with pancreatic duct carcinoma were analyzed in relation to gender and age, histological type, histological malignancy grade (G), local lymph node involvement and distant metastases.
  • Reduced expression or abnormal localization of E-cadherin and alpha-, beta- and gamma-catenins were observed in pancreatic duct carcinoma.

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  • (PMID = 20529828.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / CDH1 protein, human; 0 / Cadherins; 0 / Catenins; 0 / alpha Catenin; 0 / beta Catenin; 0 / gamma Catenin
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45. Ji Y, Kuang TT, Tan YS, Chen Y, Zeng HY, Jin DY: Pancreatic primary lymphoma: a case report and review of the literature. Hepatobiliary Pancreat Dis Int; 2005 Nov;4(4):622-6
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  • [Title] Pancreatic primary lymphoma: a case report and review of the literature.
  • BACKGROUND: Primary pancreatic lymphoma is a rare but treatable malignancy (less than 1% of pancreatic tumors) that may be clinically confused with pancreatic adenocarcinoma.
  • METHODS: In a patient with upper abdominal pain, ultrasonography and CT detected a mass in pancreatic head, which compressed the common bile duct.
  • RESULTS: Grossly the tumor involved the pancreatic head, soft in consistence and invaded part of the gastric wall.
  • Histologically, the tumor was composed mainly of large and moderate neoplastic cells, which were diffusely positive for CD20 and Bcl-6 antigens, indicating the features of diffusely large B cell lymphoma.
  • [MeSH-major] Lymphoma / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 16286277.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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46. Daniel SV, Vani DH, Smith AM, Hill QA, Menon KV: Obstructive jaundice due to a pancreatic mass: a rare presentation of acute lymphoblastic leukaemia in an adult. JOP; 2010;11(1):72-4
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  • [Title] Obstructive jaundice due to a pancreatic mass: a rare presentation of acute lymphoblastic leukaemia in an adult.
  • Liver function tests showed an obstructive picture, full blood count was normal and on computerised tomography there was diffuse enlargement of the pancreas, with dilatation of the common bile duct and intra hepatic biliary radicles.
  • Four weeks after presenting, the white cell count became elevated with blasts on the blood film and bone marrow biopsy revealed a precursor B cell acute lymphoblastic leukaemia.
  • After induction chemotherapy his jaundice resolved, the pancreatic mass reduced in size and he is now in a complete remission.
  • CONCLUSION: Acute lymphoblastic leukaemia may mimic common causes of a pancreatic mass such as adenocarcinoma and should be considered as part of the differential diagnosis when atypical features are present.
  • [MeSH-major] Jaundice, Obstructive / diagnosis. Pancreatic Diseases / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male. Organ Size. Pancreas / pathology

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  • (PMID = 20065559.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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47. Hayashi A, Aishima S, Miyasaka Y, Nakata K, Morimatsu K, Oda Y, Nagai E, Oda Y, Tanaka M, Tsuneyoshi M: Pdcd4 expression in intraductal papillary mucinous neoplasm of the pancreas: its association with tumor progression and proliferation. Hum Pathol; 2010 Nov;41(11):1507-15
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  • [Title] Pdcd4 expression in intraductal papillary mucinous neoplasm of the pancreas: its association with tumor progression and proliferation.
  • Intraductal papillary mucinous neoplasm is characterized by cystically dilated main and/or branch pancreatic duct with mucus.
  • Programmed cell death 4 is a recently identified tumor suppressor that was found to inhibit translation.
  • Programmed cell death 4 has been reported to inhibit tumorigenesis, tumor progression, proliferation, invasion, and metastasis in several human malignancies.
  • We examined 108 cases of intraductal papillary mucinous neoplasm by immunohistochemistry and revealed that programmed cell death 4 expression was recognized in both the nucleus and cytoplasm in intraductal papillary mucinous neoplasm.
  • The positive rate of programmed cell death 4 was 79%, 43%, and 10% in adenoma, borderline, and carcinoma, respectively.
  • The positive rate of programmed cell death 4 decreased from adenoma to carcinoma (P < .0001, both adenoma versus borderline and borderline versus carcinoma), indicating that programmed cell death 4 might inhibit tumor progression in intraductal papillary mucinous neoplasm.
  • Programmed cell death 4 expression had a strong relationship with p21 expression (P < .0001) and an inverse correlation with Ki-67 labeling index (r = -0.6255, P < .0001).
  • Thus, programmed cell death 4 might inhibit the proliferation of intraductal papillary mucinous neoplasm; and its inhibition might partly result from cell cycle arrest caused by the up-regulation of p21.
  • In conclusion, programmed cell death 4 may inhibit tumor progression in intraductal papillary mucinous neoplasm; and the loss of programmed cell death 4 expression is representative of the malignant potential of intraductal papillary mucinous neoplasm including the proliferative activity.
  • Therefore, programmed cell death 4 can be an important biomarker for intraductal papillary mucinous neoplasm.
  • [MeSH-major] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Papillary / metabolism. Apoptosis Regulatory Proteins / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Ducts / pathology. Pancreatic Neoplasms / metabolism. RNA-Binding Proteins / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / mortality. Adenoma / pathology. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cell Proliferation. Cytoplasm / metabolism. Cytoplasm / pathology. Disease Progression. Fluorescent Antibody Technique, Direct. Humans. Japan / epidemiology. Ki-67 Antigen / metabolism. Survival Rate

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  • [Copyright] Copyright © 2010. Published by Elsevier Inc.
  • (PMID = 20656320.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / PDCD4 protein, human; 0 / RNA-Binding Proteins
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48. Tanno S, Obara T, Koizumi K, Nakano Y, Osanai M, Mizukami Y, Kohgo Y: Risk of additional pancreatic cancer in patients with branch duct intraductal papillary-mucinous neoplasm. Clin J Gastroenterol; 2009 Dec;2(6):365-370
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  • [Title] Risk of additional pancreatic cancer in patients with branch duct intraductal papillary-mucinous neoplasm.
  • Branch duct intraductal papillary-mucinous neoplasms of the pancreas (BD-IPMN) are being diagnosed with increasing frequency.
  • Although BD-IPMN outcomes are generally good, pancreatic ductal adenocarcinoma (PDA) is found distant from the original BD-IPMN in about 3.3-9.2% of cases.
  • Recent findings from follow-up studies suggest that pancreases with BD-IPMNs have a high risk of developing additional pancreatic cancer, with standardized incidence ratios (SIRs) of 15.8- to 26-fold.

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  • [Cites] J Hepatobiliary Pancreat Surg. 2007;14(3):255-63 [17520200.001]
  • [Cites] N Engl J Med. 1992 Mar 12;326(11):737-40 [1445507.001]
  • [Cites] Gut. 2006 Nov;55(11):1533-5 [17047104.001]
  • [Cites] Pancreas. 2010 Jan;39(1):36-40 [19745777.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):977-87 [15252303.001]
  • [Cites] Virchows Arch. 1994;425(4):357-67 [7820300.001]
  • [Cites] Ann Surg. 2004 Jun;239(6):788-97; discussion 797-9 [15166958.001]
  • [Cites] Science. 1996 May 24;272(5265):1187-90 [8638166.001]
  • [Cites] Arch Surg. 2003 Apr;138(4):427-3; discussion 433-4 [12686529.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):4071-4 [8395336.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2140-3 [9187111.001]
  • [Cites] Gut. 1996 Sep;39(3):457-64 [8949654.001]
  • [Cites] Pancreatology. 2006;6(1-2):17-32 [16327281.001]
  • [Cites] Gastroenterol Clin North Am. 2007 Dec;36(4):831-49, vi [17996793.001]
  • [Cites] Gastroenterology. 1991 Aug;101(2):512-9 [1648527.001]
  • [Cites] Gastroenterology. 1996 Jan;110(1):227-31 [8536861.001]
  • [Cites] Am J Surg Pathol. 1995 May;19(5):576-89 [7726368.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):72-9; quiz 309-10 [17631133.001]
  • [Cites] Cancer. 2001 Oct 1;92(7):1807-17 [11745253.001]
  • [Cites] Gut. 2007 Aug;56(8):1086-90 [17127707.001]
  • [Cites] Am J Gastroenterol. 1991 Nov;86(11):1619-25 [1659183.001]
  • [Cites] Ann Surg. 1997 Oct;226(4):491-8; discussion 498-500 [9351717.001]
  • [Cites] Cancer. 1991 Feb 1;67(3):634-7 [1845953.001]
  • [Cites] J Surg Oncol. 1994 Feb;55(2):84-91 [8121190.001]
  • [Cites] Arch Surg. 2002 Nov;137(11):1274-8 [12413317.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Oct;4(10):1265-70 [16979953.001]
  • [Cites] Jpn J Cancer Res. 1991 Oct;82(10):1057-60 [1955373.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Gastroenterology. 1996 Jun;110(6):1909-18 [8964418.001]
  • [Cites] Hum Pathol. 1997 Sep;28(9):1010-7 [9308724.001]
  • [Cites] J Pathol. 1998 Dec;186(4):363-71 [10209484.001]
  • [Cites] Gut. 2008 Mar;57(3):339-43 [17660227.001]
  • [Cites] Pancreatology. 2002;2(5):484-90 [12378117.001]
  • [Cites] Pancreatology. 2010;10(2-3):173-8 [20484955.001]
  • [Cites] Hum Pathol. 1992 Jan;23(1):82-5 [1312058.001]
  • [Cites] Ann Surg. 2001 Sep;234(3):313-21; discussion 321-2 [11524584.001]
  • [Cites] Ann Surg. 1997 Jun;225(6):637-44; discussion 644-6 [9230804.001]
  • [Cites] Cancer. 1991 Jul 1;68(1):159-68 [2049738.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Jun;7(6):515-21 [9641496.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):266-79 [17785207.001]
  • [Cites] HPB (Oxford). 2001;3(4):257-62 [18333027.001]
  • [Cites] Ann Surg. 2004 May;239(5):678-85; discussion 685-7 [15082972.001]
  • [Cites] Int J Pancreatol. 1995 Aug;18(1):1-6 [7594765.001]
  • [Cites] Gut. 2008 Nov;57(11):1561-5 [18477671.001]
  • [Cites] Cancer. 2002 Jan 1;94(1):62-77 [11815961.001]
  • [Cites] World J Surg. 1993 Jan-Feb;17(1):122-6; discussion 126-7 [8383381.001]
  • [Cites] J Gastroenterol. 2005 Jul;40(7):669-75 [16082582.001]
  • [Cites] Surgery. 2003 May;133(5):459-63 [12773972.001]
  • [Cites] Cancer Res. 1993 Mar 1;53(5):953-6 [8439969.001]
  • [Cites] Jpn J Cancer Res. 1999 Aug;90(8):841-8 [10543256.001]
  • [Cites] J Gastroenterol. 2005 Jul;40(7):744-51 [16082592.001]
  • [Cites] Am J Surg. 1998 May;175(5):426-32 [9600293.001]
  • [Cites] Cancer. 1989 Sep 15;64(6):1329-35 [2548703.001]
  • [Cites] Ann Surg. 1993 Feb;217(2):138-43 [8439212.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 1999;6(3):281-5 [10526064.001]
  • [Cites] Jpn J Clin Oncol. 2002 Apr;32(4):146-51 [12072425.001]
  • [Cites] Am J Surg Pathol. 2004 Sep;28(9):1184-92 [15316318.001]
  • [Cites] Ann Surg. 2007 Oct;246(4):644-51; discussion 651-4 [17893501.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4740-4 [9788631.001]
  • (PMID = 26192788.001).
  • [ISSN] 1865-7257
  • [Journal-full-title] Clinical journal of gastroenterology
  • [ISO-abbreviation] Clin J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Branch duct / Follow-up / IPMN / Pancreatic cancer / Risk factor
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49. Logsdon CD, Ji B: Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer. Clin Gastroenterol Hepatol; 2009 Nov;7(11 Suppl):S40-3
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  • [Title] Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.
  • The relationship between chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) is unclear.
  • However, it has been long thought that PDAC arises only from duct cells.
  • However, we have recently found that excessive activity within the Ras signaling pathway can lead to acinar cell death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from acinar cells through the full complement of preneoplastic (pancreatic intraepithelial neoplasia) lesions.

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  • [Cites] Hepatogastroenterology. 1999 Jan-Feb;46(25):31-7 [10228761.001]
  • [Cites] Am J Surg. 1997 Sep;174(3):242-6 [9324130.001]
  • [Cites] Neoplasia. 2005 Jan;7(1):17-23 [15720814.001]
  • [Cites] Adv Anat Pathol. 2005 Mar;12(2):81-91 [15731576.001]
  • [Cites] Biochim Biophys Acta. 2005 Nov 25;1756(2):97-101 [16169155.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2165-78 [16762637.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Adv Med Sci. 2006;51:23-30 [17357272.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42 [17360542.001]
  • [Cites] Gastroenterology. 2007 Apr;132(4):1557-73 [17466744.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):266-79 [17785207.001]
  • [Cites] Annu Rev Pathol. 2008;3:157-88 [18039136.001]
  • [Cites] Neoplasia. 2008 Aug;10(8):782-96 [18670639.001]
  • [Cites] Biochem Biophys Res Commun. 2009 May 8;382(3):561-5 [19292977.001]
  • [Cites] Gastroenterology. 2009 Sep;137(3):1072-82, 1082.e1-6 [19501586.001]
  • [Cites] Int J Pancreatol. 2000 Apr;27(2):93-103 [10862508.001]
  • [Cites] Genes Dev. 2001 Feb 1;15(3):286-93 [11159909.001]
  • [Cites] Mod Pathol. 2002 Apr;15(4):441-7 [11950919.001]
  • [Cites] Gut. 2002 Dec;51(6):849-52 [12427788.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2005-9 [12727809.001]
  • [Cites] Mod Pathol. 2003 Oct;16(10):996-1006 [14559982.001]
  • [Cites] Pancreas. 2003 Nov;27(4):297-300 [14576490.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1495-501 [14657708.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] World J Gastroenterol. 2004 Mar 15;10(6):881-4 [15040037.001]
  • [Cites] Endoscopy. 2004 Jun;36(6):535-42 [15202051.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Aug;287(2):G315-9 [15246966.001]
  • [Cites] Virchows Arch A Pathol Anat Histol. 1982 Aug;396(3):331-49 [7135827.001]
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] Acta Cytol. 1989 Nov-Dec;33(6):870-4 [2588919.001]
  • [Cites] N Engl J Med. 1993 May 20;328(20):1433-7 [8479461.001]
  • [Cites] Am J Gastroenterol. 1993 Oct;88(10):1700-4 [8213710.001]
  • [Cites] J Natl Cancer Inst. 1994 Apr 20;86(8):625-7 [8145277.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2761-4 [8168108.001]
  • [Cites] Am J Pathol. 1994 Dec;145(6):1547-50 [7992857.001]
  • [Cites] N Engl J Med. 1995 Jun 1;332(22):1482-90 [7739686.001]
  • [Cites] Gastroenterology. 1995 Jul;109(1):247-51 [7797022.001]
  • [Cites] Ann Intern Med. 1995 Aug 1;123(3):188-91 [7598300.001]
  • [Cites] Am J Physiol. 1995 Jun;268(6 Pt 1):G1060-5 [7611406.001]
  • [Cites] Cancer Res. 1995 Oct 1;55(19):4264-7 [7671233.001]
  • [Cites] J Natl Cancer Inst. 1997 Mar 19;89(6):442-6 [9091646.001]
  • [Cites] Neoplasma. 2004;51(5):400-4 [15640947.001]
  • (PMID = 19896097.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / DK052067
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 46
  • [Other-IDs] NLM/ NIHMS268542; NLM/ PMC3050544
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50. Schneider A, Löhr JM: [Autoimmune pancreatitis]. Internist (Berl); 2009 Mar;50(3):318-30
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  • Morphological hallmarks of the disease are narrowing of the pancreatic duct system and the bile duct by periductal lymphoplasmocytic inflammation.
  • This results in many cases in obstructive jaundice due to a mass-forming lesion in the pancreatic head mimicking pancreatic ductal adenocarcinoma.
  • Autoimmune pancreatitis will respond to steroid treatment, which is of specific importance because pancreatic cancer is one of its clinical differential diagnoses.

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  • [Cites] J Gastroenterol. 2006 Jul;41(7):613-25 [16932997.001]
  • [Cites] Dig Dis Sci. 1995 Jul;40(7):1561-8 [7628283.001]
  • [Cites] Gastrointest Endosc. 2004 Dec;60(6):937-44 [15605009.001]
  • [Cites] Hepatol Res. 2007 Oct;37 Suppl 3:S487-95 [17931208.001]
  • [Cites] Lab Invest. 2005 Oct;85(10):1276-91 [16127427.001]
  • [Cites] Am J Surg Pathol. 2004 Sep;28(9):1193-203 [15316319.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):631-3 [17372266.001]
  • [Cites] Am J Gastroenterol. 2004 May;99(5):884-8 [15128355.001]
  • [Cites] Gastroenterology. 1996 May;110(5):1579-86 [8613065.001]
  • [Cites] Baillieres Clin Gastroenterol. 1998 Jun;12(2):293-315 [9890074.001]
  • [Cites] J Gastroenterol. 2003;38(12 ):1155-61 [14714253.001]
  • [Cites] Am J Gastroenterol. 2007 Jan;102(1):220-1 [17278279.001]
  • [Cites] World J Gastroenterol. 2002 Apr;8(2):301-4 [11925612.001]
  • [Cites] Dig Dis Sci. 1985 Dec;30(12):1121-6 [2866072.001]
  • [Cites] Am J Surg Pathol. 2007 Apr;31(4):521-8 [17414098.001]
  • [Cites] Virchows Arch. 2004 Dec;445(6):552-63 [15517359.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1787-98 [12000730.001]
  • [Cites] BMC Genomics. 2008 Jul 29;9:354 [18664271.001]
  • [Cites] Gastroenterology. 2007 Apr;132(4):1557-73 [17466744.001]
  • [Cites] Pancreas. 2007 Oct;35(3):281-4 [17895852.001]
  • [Cites] World J Gastroenterol. 2006 Jul 14;12 (26):4181-4 [16830370.001]
  • [Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S113-31 [17486047.001]
  • [Cites] Gastroenterology. 1998 Aug;115(2):421-32 [9679048.001]
  • [Cites] Radiology. 2004 Nov;233(2):345-52 [15459324.001]
  • [Cites] N Engl J Med. 2001 Mar 8;344(10):732-8 [11236777.001]
  • [Cites] J Gastroenterol. 2007 May;42 Suppl 18:39-41 [17520222.001]
  • [Cites] Gut. 1998 Jul;43(1):128-33 [9771417.001]
  • [Cites] Lancet. 2000 Sep 9;356(9233):910-1 [11036899.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Aug;4(8):1010-6; quiz 934 [16843735.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):368-9 [17631165.001]
  • [Cites] J Cell Mol Med. 2005 Jul-Sep;9(3):741-4 [16202223.001]
  • [Cites] Am J Gastroenterol. 2007 Nov;102(11):2417-25 [17894845.001]
  • [Cites] Pancreas. 2003 Jul;27(1):14-9 [12826900.001]
  • [Cites] Cancer. 2002 Nov 1;95(9):1946-53 [12404289.001]
  • [Cites] Am J Surg Pathol. 2008 Jul;32(7):986-95 [18460977.001]
  • [Cites] J Ultrasound Med. 2004 Feb;23 (2):199-206 [14992356.001]
  • [Cites] Immunology. 2002 Jan;105(1):9-19 [11849310.001]
  • [Cites] J Gastroenterol. 2008;43(6):403-8 [18600383.001]
  • [Cites] Am J Surg Pathol. 2003 Aug;27(8):1119-27 [12883244.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Oct;5(10):1229-34 [17702660.001]
  • [Cites] N Engl J Med. 2007 Apr 12;356(15):1587; author reply 1587 [17436434.001]
  • [Cites] J Gastroenterol. 2007 Jan;42 Suppl 17:55-7 [17238028.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1992;421(5):371-8 [1360719.001]
  • [Cites] Chirurg. 2006 Feb;77(2):154-65 [16208510.001]
  • [Cites] Am J Gastroenterol. 2005 Dec;100(12 ):2808-13 [16393239.001]
  • [Cites] Gut. 2002 Jul;51(1):1-4 [12077078.001]
  • [Cites] Am J Gastroenterol. 2000 Sep;95(9):2391-4 [11007255.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2006 May;3(5):236-7 [16672986.001]
  • [Cites] Hum Pathol. 1991 Apr;22(4):387-95 [2050373.001]
  • [Cites] Am J Surg Pathol. 2003 Mar;27(3):334-42 [12604889.001]
  • [Cites] Gastrointest Endosc. 2005 Mar;61(3):467-72 [15758927.001]
  • [Cites] Gut. 1997 Aug;41(2):263-8 [9301509.001]
  • [Cites] J Antimicrob Chemother. 2002 Nov;50(5):639-47 [12407119.001]
  • [Cites] Lab Invest. 2002 Apr;82(4):411-24 [11950899.001]
  • [Cites] J Gastrointest Surg. 2003 Jan;7(1):129-37; discussion 137-9 [12559194.001]
  • [Cites] Gut. 2006 Sep;55(9):1361-2 [16905703.001]
  • [Cites] Histopathology. 2005 Aug;47(2):147-58 [16045775.001]
  • [Cites] Virchows Arch. 2004 Jul;445(1):1-8 [15138818.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Nov;5(11):1347-53 [17702659.001]
  • [Cites] Scand J Gastroenterol. 1999 Feb;34(2):199-201 [10192201.001]
  • [Cites] J Gastroenterol. 2007 Jul;42(7):550-9 [17653651.001]
  • [Cites] J Gastroenterol. 2003;38(10):982-4 [14614606.001]
  • [Cites] Gastrointest Endosc. 2002 Apr;55(4):494-9 [11923760.001]
  • [Cites] Am J Surg. 1984 Jun;147(6):822-6 [6731702.001]
  • [Cites] Am J Surg Pathol. 2003 Apr;27(4):441-51 [12657928.001]
  • [Cites] Am J Dig Dis. 1961 Jul;6:688-98 [13746542.001]
  • [Cites] Intern Med. 2005 Aug;44(8):886-91 [16157994.001]
  • [Cites] Pancreatology. 2001;1(3):246-53 [12120203.001]
  • [Cites] Mod Pathol. 2007 Jan;20(1):23-8 [16980948.001]
  • [Cites] J Cell Mol Med. 2005 Jan-Mar;9(1):196-207 [15784177.001]
  • [Cites] JOP. 2005 Jul 08;6(4):382-405 [16006694.001]
  • [Cites] AJR Am J Roentgenol. 1998 May;170(5):1323-7 [9574610.001]
  • [Cites] J Clin Invest. 2000 Apr;105(8):1057-65 [10772650.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2007 Jun;4(6):314-23 [17541445.001]
  • [Cites] Gut. 2007 Dec;56(12):1650-2 [17998320.001]
  • [Cites] Am J Gastroenterol. 2004 Aug;99(8):1605-16 [15307882.001]
  • [Cites] Immunogenetics. 2007 Jan;59(1):45-52 [17119950.001]
  • [Cites] Z Gastroenterol. 2006 Dec;44(12):1227-9 [17163373.001]
  • [Cites] Clin Immunol. 2003 Nov;109(2):212-23 [14597220.001]
  • [Cites] BMC Med. 2006 Oct 06;4:23 [17026742.001]
  • [Cites] Gastrointest Endosc. 2007 Dec;66(6):1142-51 [18061714.001]
  • [Cites] Pancreas. 2005 Apr;30(3):272-8 [15782107.001]
  • [Cites] Gastrointest Endosc. 2004 Dec;60(6):927-36 [15605008.001]
  • [Cites] Pancreas. 2006 Jul;33(1):20-6 [16804408.001]
  • [Cites] N Engl J Med. 2006 Dec 21;355(25):2670-6 [17182992.001]
  • [Cites] Pancreas. 2003 Jul;27(1):26-30 [12826902.001]
  • [Cites] Pathologe. 2005 Feb;26(1):67-72 [15630570.001]
  • [Cites] Semin Ultrasound CT MR. 2007 Oct;28(5):384-94 [17970554.001]
  • [Cites] J Gastroenterol. 2007 May;42 Suppl 18:28-31 [17520220.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):573-81 [10702209.001]
  • [Cites] Pancreatology. 2005;5(2-3):234-8; discussion 238-40 [15855821.001]
  • [Cites] Gastroenterology. 2002 May;122(5):1264-9 [11984513.001]
  • [Cites] Gastrointest Endosc. 2007 Dec;66(6):1152-3 [18061715.001]
  • [Cites] Pathologe. 1988 Mar;9(2):103-8 [3283722.001]
  • [Cites] Lancet. 2001 Mar 10;357(9258):752-6 [11253969.001]
  • [Cites] Lab Invest. 2000 Jan;80(1):47-55 [10653002.001]
  • [Cites] Pancreas. 2005 Jan;30(1):31-9 [15632697.001]
  • [Cites] Pancreas. 2005 Oct;31(3):232-7 [16163054.001]
  • [Cites] Am J Surg Pathol. 2006 Dec;30(12):1537-45 [17122509.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):78-82 [18059268.001]
  • [Cites] Acta Med Scand. 1979;205(1-2):139-41 [760402.001]
  • [Cites] Pancreas. 2003 Jan;26(1):92-4 [12499924.001]
  • [Cites] Gut. 2005 May;54(5):703-9 [15831920.001]
  • [Cites] Mol Cancer. 2003 Jan 06;2:4 [12556242.001]
  • [Cites] Pancreatology. 2002;2(6):550-6 [12435868.001]
  • [Cites] J Gastroenterol. 2007 Feb;42(2):101-19 [17351799.001]
  • [Cites] Pancreatology. 2005;5(2-3):300-3 [15855829.001]
  • [Cites] J Gastroenterol. 2007 Jan;42 Suppl 17:66-71 [17238031.001]
  • [Cites] Pancreas. 2007 Apr;34(3):279-86 [17414049.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Aug;291(2):G345-54 [16825661.001]
  • [Cites] Am J Gastroenterol. 2000 Oct;95(10):2788-94 [11051349.001]
  • [Cites] Pancreas. 2005 Mar;30(2):192-3 [15714146.001]
  • [Cites] Am J Gastroenterol. 2007 Aug;102(8):1646-53 [17555461.001]
  • [Cites] Pancreas. 2007 Aug;35(2):156-61 [17632322.001]
  • [Cites] Pancreas. 2003 Jul;27(1):1-13 [12826899.001]
  • [Cites] Int J Pancreatol. 1988 Mar;3(2-3):185-93 [3361159.001]
  • [Cites] Hepatology. 2007 Aug;46(2):463-71 [17634963.001]
  • [Cites] Eur J Nucl Med. 2000 Dec;27(12 ):1835-8 [11189947.001]
  • [Cites] Intern Med. 2007;46(17):1365-71 [17827834.001]
  • [Cites] Gastroenterology. 2001 Feb;120(3):682-707 [11179244.001]
  • [Cites] Gut. 2007 Dec;56(12):1719-24 [17525092.001]
  • (PMID = 19212732.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics
  • [Number-of-references] 133
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51. Hanley S, Rosenberg L: Transforming growth factor beta is a critical regulator of adult human islet plasticity. Mol Endocrinol; 2007 Jun;21(6):1467-77
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  • Tissue plasticity is well documented in the context of pancreatic regeneration and carcinogenesis, with recent reports implicating dedifferentiated islet cells both as endocrine progenitors and as the cell(s) of origin in pancreatic adenocarcinoma.
  • Accordingly, it is noteworthy that accumulating evidence suggests that TGFbeta signaling is essential to pancreatic endocrine development and maintenance, whereas its loss is associated with the progression to pancreatic adenocarcinoma.
  • Human islets were embedded in a collagen gel and cultured under conditions that induced transformation into duct-like epithelial structures (DLS).
  • Localization of TGFbeta signaling molecules suggested that the action of TGFbeta is directly on the beta-cell to inhibit apoptosis and thus stabilize endocrine phenotype.
  • [MeSH-minor] Adult. Cell Differentiation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. MAP Kinase Kinase 4 / metabolism. Pancreatic Ducts / cytology. Pancreatic Ducts / growth & development. Receptors, Transforming Growth Factor beta / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 17405902.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4
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52. Peng SY, Hong DF, Liu YB, Li JT, Tao F, Tan ZJ: [A pancreas suture-less type II binding pancreaticogastrostomy]. Zhonghua Wai Ke Za Zhi; 2009 Dec 1;47(23):1764-6
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  • [Title] [A pancreas suture-less type II binding pancreaticogastrostomy].
  • OBJECTIVE: To explore the feasibility and safety of type II binding pancreaticogastrostomy (BPG) in pancreaticoduodenectomy and mid-segmentectomy of pancreas.
  • METHODS: From November 2008 to May 2009, 26 patients underwent pancreaticoduodenectomy and mid-segmentectomy of pancreas with type II BPG reconstruction, including 13 cases of pancreatic head cancer, 3 cases of duodenal adenocarcinoma, 2 cases of ampullary carcinoma, 4 cases of cholangiocarcinoma, 1 case of bile duct cell severe atypical hyperplasia, and 1 case of stomach cancer.
  • The process of type II BPG was described as the following: after pancreas remnant was mobilized for 2-3 cm, a piece of sero-muscular layer at the posterior gastric wall was excised and then a sero-muscular depth purse-suturing with 3-0 prolene was pre-placed (outer purse-string).
  • Through the two pre-placed purse-strings, the pancreas remnant was pulled into the gastric lumen and then posterior gastric wall was pushed backward to keep it closely in contact with the retro-peritoneal wall.
  • No mortality or pancreatic leakage occurred.
  • CONCLUSIONS: Pancreaticogastrostomy is good for accommodating a large pancreas stump.
  • [MeSH-major] Anastomosis, Surgical / methods. Pancreas / surgery. Stomach / surgery

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  • (PMID = 20193541.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] China
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53. Seeley ES, Carrière C, Goetze T, Longnecker DS, Korc M: Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia. Cancer Res; 2009 Jan 15;69(2):422-30
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  • [Title] Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia.
  • In this study, we determined that ciliogenesis is suppressed in both pancreatic cancer cells and pancreatic intraepithelial neoplasia (PanIN) lesions in human pancreatic ductal adenocarcinoma (PDAC).
  • Inhibition of Kras effector pathways restored ciliogenesis in a mouse pancreatic cancer cell line, raising the possibility that ciliogenesis may be actively repressed by oncogenic Kras.
  • By contrast, normal duct, islet, and centroacinar cells retained primary cilia in both human and mouse pancreata.

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  • [Cites] Nature. 2003 Nov 6;426(6962):83-7 [14603322.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Mech Dev. 2004 Jan;121(1):3-14 [14706695.001]
  • [Cites] Gene. 2004 Mar 17;328:135-42 [15019993.001]
  • [Cites] Development. 2004 Jul;131(14):3457-67 [15226261.001]
  • [Cites] Genes Dev. 2004 Jul 1;18(13):1630-42 [15231740.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):977-87 [15252303.001]
  • [Cites] J Cell Biol. 1971 Apr;49(1):226-9 [5555577.001]
  • [Cites] Cell. 1979 Jul;17(3):527-35 [476831.001]
  • [Cites] J Ultrastruct Res. 1979 Aug;68(2):173-85 [480410.001]
  • [Cites] Acta Pathol Jpn. 1983 Mar;33(2):297-321 [6346783.001]
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] Science. 1994 May 27;264(5163):1329-33 [8191288.001]
  • [Cites] Am J Pathol. 1996 Dec;149(6):1919-30 [8952527.001]
  • [Cites] Oncogene. 1997 Oct 9;15(15):1797-803 [9362446.001]
  • [Cites] Surg Oncol Clin N Am. 1998 Jan;7(1):25-41 [9443985.001]
  • [Cites] J Cell Biol. 1998 May 18;141(4):993-1008 [9585417.001]
  • [Cites] Histol Histopathol. 1999 Apr;14(2):539-52 [10212816.001]
  • [Cites] Hepatology. 1999 Sep;30(3):677-81 [10462374.001]
  • [Cites] Neoplasma. 2004;51(5):400-4 [15640947.001]
  • [Cites] J Cell Sci. 2005 Aug 1;118(Pt 15):3317-26 [16030138.001]
  • [Cites] Invest New Drugs. 2005 Oct;23(5):485-7 [16133800.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1960-6 [17452677.001]
  • [Cites] Cell. 2007 Jun 1;129(5):855-7 [17540164.001]
  • [Cites] Am J Pathol. 2007 Jul;171(1):263-73 [17591971.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1351-63 [17604723.001]
  • [Cites] Science. 2007 Jul 20;317(5836):372-6 [17641202.001]
  • [Cites] Cell. 2007 Aug 24;130(4):678-90 [17719545.001]
  • [Cites] PLoS One. 2007;2(11):e1155 [17982507.001]
  • [Cites] Gastroenterology. 2007 Dec;133(6):1999-2009 [18054571.001]
  • [Cites] Dev Dyn. 2008 Aug;237(8):2039-52 [18629868.001]
  • [Cites] Mol Cancer Ther. 2008 Sep;7(9):2725-35 [18790753.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):1821-5 [10854204.001]
  • [Cites] J Cell Biol. 2000 Oct 30;151(3):709-18 [11062270.001]
  • [Cites] Biochem J. 2000 Oct 1;351(Pt 1):95-105 [10998351.001]
  • [Cites] J Membr Biol. 2001 Nov 1;184(1):71-9 [11687880.001]
  • [Cites] Mod Pathol. 2002 Apr;15(4):441-7 [11950919.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(18):8285-98 [16135816.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):185-95 [16169464.001]
  • [Cites] Curr Biol. 2005 Oct 25;15(20):1861-6 [16243034.001]
  • [Cites] PLoS Genet. 2005 Oct;1(4):e53 [16254602.001]
  • [Cites] J Am Soc Nephrol. 2005 Dec;16(12):3485-9 [16267153.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Genes Dev. 2006 May 15;20(10):1218-49 [16702400.001]
  • [Cites] Drugs. 2006;66(8):1059-72 [16789792.001]
  • [Cites] J Am Soc Nephrol. 2006 Jul;17(7):1801-6 [16775032.001]
  • [Cites] Cancer Res. 2006 Jul 15;66(14):6903-7 [16849532.001]
  • [Cites] Gastroenterology. 2006 Dec;131(6):1856-69 [17123526.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Nat Cell Biol. 2007 Feb;9(2):160-70 [17330329.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42 [17360542.001]
  • [Cites] Nat Cell Biol. 2007 May;9(5):493-505 [17450133.001]
  • [Cites] J Biol Chem. 2007 May 11;282(19):14048-55 [17353198.001]
  • (PMID = 19147554.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102687-05; United States / NCI NIH HHS / CA / CA-102687; United States / NCI NIH HHS / CA / R01 CA102687; United States / NCI NIH HHS / CA / CA-127095; United States / NCI NIH HHS / CA / R01 CA102687-05; United States / NCI NIH HHS / CA / CA-101306; United States / NCI NIH HHS / CA / R21 CA127095; United States / NCI NIH HHS / CA / R01 CA075059; United States / NCI NIH HHS / CA / CA101306-05; United States / NCI NIH HHS / CA / R01 CA101306; United States / NCI NIH HHS / CA / R01 CA101306-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS79339; NLM/ PMC2629528
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54. Shimizu K, Kitahashi T, Fujii H, Tsutsumi M, Mori T, Honoki K, Tsujiuchi T: Alterations in the Smad4 gene in hamster pancreatic duct adenocarcinomas and established cell lines. Oncol Rep; 2006 Jul;16(1):85-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alterations in the Smad4 gene in hamster pancreatic duct adenocarcinomas and established cell lines.
  • Alterations of the Smad4 gene, identified as a mediator of the transforming growth factor-beta pathway, were investigated in hamster pancreatic duct adenocarcinomas (PDAs) and established cell lines.
  • A total of 12 PDAs obtained 10 weeks after beginning the experiment and three cell lines established from subcutaneously transplantable PDAs in syngeneic hamsters were examined for mutations using reverse transcription-polymerase chain reaction-single strand conformation polymorphism (RT-PCR-SSCP) analysis.
  • A mutation was detected in only one PDA (1/12, 8.3%) in the form of an ACC to ATC (Thr to IIe) transition at codon 73; none were detected in the three cell lines.
  • These results suggest that the Smad4 gene might play a role in limited fraction of BOP-induced pancreatic duct carcinogenesis in hamsters.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Pancreatic Ductal / genetics. Gene Expression Regulation, Neoplastic. Smad4 Protein / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cricetinae. Female. Genetic Predisposition to Disease. Mesocricetus. Nitrosamines. Polymorphism, Single-Stranded Conformational. RNA / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16786127.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Nitrosamines; 0 / Smad4 Protein; 60599-38-4 / nitrosobis(2-oxopropyl)amine; 63231-63-0 / RNA
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55. Nielsen SK, Møllgård K, Clement CA, Veland IR, Awan A, Yoder BK, Novak I, Christensen ST: Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines. Dev Dyn; 2008 Aug;237(8):2039-52
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  • [Title] Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines.
  • Hedgehog (Hh) signaling controls pancreatic development and homeostasis; aberrant Hh signaling is associated with several pancreatic diseases.
  • Here we investigated the link between Hh signaling and primary cilia in the human developing pancreatic ducts and in cultures of human pancreatic duct adenocarcinoma cell lines, PANC-1 and CFPAC-1.
  • We show that the onset of Hh signaling from human embryogenesis to fetal development is associated with accumulation of Hh signaling components Smo and Gli2 in duct primary cilia and a reduction of Gli3 in the duct epithelium.
  • These findings indicate that primary cilia are involved in pancreatic development and postnatal tissue homeostasis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Cilia / metabolism. Hedgehog Proteins / metabolism. Pancreas / cytology. Pancreas / embryology. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Epithelial Cells / metabolism. Epithelial Cells / ultrastructure. Female. Fetus / cytology. Green Fluorescent Proteins / genetics. Humans. Kruppel-Like Transcription Factors / genetics. Kruppel-Like Transcription Factors / metabolism. Mice. NIH 3T3 Cells. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Pregnancy. Receptors, Cell Surface / metabolism. Receptors, G-Protein-Coupled. Transfection

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  • [Copyright] Copyright (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18629868.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 R01-HD056030
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI2 protein, human; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Nuclear Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / SHH protein, human; 0 / SMO protein, human; 0 / patched receptors; 147336-22-9 / Green Fluorescent Proteins
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56. Radulovich N, Pham NA, Strumpf D, Leung L, Xie W, Jurisica I, Tsao MS: Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma. Mol Cancer; 2010 Feb 01;9:24
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  • [Title] Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma.
  • BACKGROUND: The cyclin D1 (CCND1) and cyclin D3 (CCND3) are frequently co-overexpressed in pancreatic ductal adenocarcinoma (PDAC).
  • RESULTS: CCND1 and CCND3 expression were selectively suppressed by shRNA in PDAC cell lines with expression levels of equal CCND1 and CCND3 (BxPC3), enhanced CCND1 (HPAC) or enhanced CCND3 (PANC1).
  • Suppression of cell proliferation was greater with CCND3 than CCND1 downregulation.
  • The downregulated gene targets in CCND3 suppressed cells were significantly enriched in cell cycle associated processes (p < 0.005).
  • CONCLUSIONS: Our results suggest that CCND3 is the primary driver of the cell cycle, in cooperation with CCND1 that integrates extracellular mitogenic signaling.
  • We also present evidence that CCND1 plays a role in tumor cell migration.
  • The results provide novel insights for common and differential targets of CCND1 and CCND3 overexpression during pancreatic duct cell carcinogenesis.

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  • [Cites] Cancer Res. 1997 Aug 1;57(15):3126-30 [9242437.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Am J Physiol. 1997 Nov;273(5 Pt 1):L941-9 [9374720.001]
  • [Cites] Langenbecks Arch Surg. 1998 Apr;383(2):105-15 [9641882.001]
  • [Cites] J Virol. 1998 Nov;72(11):8463-71 [9765382.001]
  • [Cites] Genes Dev. 2004 Nov 15;18(22):2699-711 [15545627.001]
  • [Cites] Mol Cell. 2004 Dec 3;16(5):831-7 [15574337.001]
  • [Cites] Int J Biochem Cell Biol. 2005 May;37(5):961-76 [15743671.001]
  • [Cites] Clin Cancer Res. 2005 Apr 15;11(8):3094-101 [15837765.001]
  • [Cites] BMC Bioinformatics. 2005;6:168 [15998470.001]
  • [Cites] Exp Mol Med. 2005 Aug 31;37(4):353-64 [16155412.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6626-36 [16103885.001]
  • [Cites] Cancer Metastasis Rev. 2005 Sep;24(3):383-93 [16258726.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D354-7 [16381885.001]
  • [Cites] Growth Factors. 2006 Mar;24(1):13-9 [16393691.001]
  • [Cites] Cell Cycle. 2006 Jan;5(1):61-70 [16294008.001]
  • [Cites] World J Gastroenterol. 2005 Nov 7;11(41):6543-8 [16425432.001]
  • [Cites] Mol Cancer Ther. 2006 Mar;5(3):483-93 [16546962.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(11):4240-56 [16705174.001]
  • [Cites] World J Gastroenterol. 2006 Jun 7;12(21):3344-51 [16733850.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):139-48 [17210693.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 20;104(12):5103-8 [17372229.001]
  • [Cites] Cancer. 2007 May 1;109(9):1897-904 [17377918.001]
  • [Cites] Genome Biol. 2007;8(5):R95 [17535438.001]
  • [Cites] Blood. 2007 Sep 15;110(6):1770-8 [17507662.001]
  • [Cites] J Proteome Res. 2008 Jan;7(1):339-51 [18076136.001]
  • [Cites] Biochim Biophys Acta. 2008 Apr;1780(4):743-9 [18230364.001]
  • [Cites] Cell Signal. 2008 Jun;20(6):1221-6 [18396012.001]
  • [Cites] Neoplasia. 2008 Jul;10(7):674-9 [18592007.001]
  • [Cites] Cancer Res. 2009 Apr 15;69(8):3317-24 [19351855.001]
  • [Cites] Bioinformatics. 2009 Dec 15;25(24):3327-9 [19837718.001]
  • [Cites] Cancer Gene Ther. 2010 May;17(5):325-33 [19851352.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3479-84 [10652342.001]
  • [Cites] EMBO J. 2000 Sep 1;19(17):4533-42 [10970847.001]
  • [Cites] Mol Cell Biol. 2001 Jul;21(14):4773-84 [11416152.001]
  • [Cites] J Cancer Res Clin Oncol. 2001 Jul;127(7):449-54 [11469683.001]
  • [Cites] J Biol Chem. 2001 Sep 7;276(36):33854-60 [11457838.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8830-7 [11751405.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] Genes Dev. 2002 Dec 15;16(24):3277-89 [12502747.001]
  • [Cites] Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238.001]
  • [Cites] RNA. 2003 Apr;9(4):493-501 [12649500.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1446-52 [12684418.001]
  • [Cites] Virchows Arch. 2003 Oct;443(4):508-17 [12942322.001]
  • [Cites] Oncogene. 2003 Oct 30;22(49):7781-95 [14586404.001]
  • [Cites] Nucleic Acids Res. 2003 Dec 15;31(24):e154 [14654707.001]
  • [Cites] Lancet Oncol. 2004 Jan;5(1):27-36 [14700606.001]
  • [Cites] AMIA Annu Symp Proc. 2003;:839 [14728344.001]
  • [Cites] Bioinformatics. 2004 Jun 12;20(9):1457-8 [14962929.001]
  • [Cites] J Clin Invest. 2004 Oct;114(7):963-8 [15467835.001]
  • [Cites] Clin Cancer Res. 2004 Oct 1;10(19):6598-605 [15475449.001]
  • [Cites] Oncogene. 1995 Aug 3;11(3):571-80 [7630641.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9363-7 [7568133.001]
  • [Cites] Cancer Res. 1997 Apr 15;57(8):1569-74 [9108461.001]
  • (PMID = 20113529.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-49585
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / CCND1 protein, human; 0 / CCND3 protein, human; 0 / Cyclin D3; 136601-57-5 / Cyclin D1; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2824633
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57. Sugita H, Hirota M, Ichihara A, Furuhashi S, Kihara S, Shimada S: Combined chemotherapy of irinotecan and low-dose cisplatin (I/low-P) against metastatic biliary tract cancer. J Hepatobiliary Pancreat Surg; 2006;13(5):463-7
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  • [Title] Combined chemotherapy of irinotecan and low-dose cisplatin (I/low-P) against metastatic biliary tract cancer.
  • There is no established or effective standard therapy for metastatic biliary tract cancer, resulting in poor prognosis.
  • Recently, we performed combination chemotherapy of irinotecan and low-dose cisplatin (I/low-P) for three consecutive patients with metastatic biliary tract cancer.
  • These outcomes suggest that I/low-P therapy is safe and may be worth trying as a first-line chemotherapy for patients with metastatic biliary tract cancer.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Bile Duct Neoplasms / drug therapy. Bile Duct Neoplasms / pathology. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Cisplatin / administration & dosage. Female. Gallbladder Neoplasms / drug therapy. Gallbladder Neoplasms / pathology. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Metastasis

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  • (PMID = 17013724.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 7673326042 / irinotecan; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
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58. Ringel J, Jesnowski R, Moniaux N, Lüttges J, Ringel J, Choudhury A, Batra SK, Klöppel G, Löhr M: Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma. Cancer Res; 2006 Sep 15;66(18):9045-53
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  • [Title] Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma.
  • To understand the role of ADAM17/tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) in pancreatic ductal adenocarcinoma (PDAC), we investigated its expression, function, and in vitro regulation.
  • ADAM17/TACE mRNA was expressed in 3 of 10 normal pancreatic tissues, 6 of 8 samples from patients with chronic pancreatitis, 10 of 10 PDAC tissues, and 9 of 9 pancreatic cancer cell lines, but it was absent in primary duct epithelial cells.
  • Immunohistochemical staining revealed positive cancer cells in 8 of 10 PDACs but no staining of ducts in normal pancreas.
  • ADAM17/TACE was found in 0 of 16 pancreatic intraepithelial neoplasia (PanIN)-1A lesions, 1 of 30 PanIN-1B lesions, 2 of 13 PanIN-2 lesions but, in 13 of 15 PanIN-3 lesions, associated with PDAC.
  • Western blot, flow cytometry, and confocal microscopy analyses showed the aberrant expression of ADAM17/TACE protein in pancreatic cancer cell lines.
  • Furthermore, ADAM17/TACE mRNA expression was down-regulated in pancreatic cancer cells arrested in G2-M phase as well as in a time-dependent manner after TNF-alpha and interleukin-6 incubation.
  • [MeSH-major] ADAM Proteins / biosynthesis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Cycle / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Neoplasm Invasiveness. Pancreatitis, Chronic / enzymology. Pancreatitis, Chronic / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16982746.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA772712
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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59. Schuller HM, Al-Wadei HA, Majidi M: GABA B receptor is a novel drug target for pancreatic cancer. Cancer; 2008 Feb 15;112(4):767-78
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  • [Title] GABA B receptor is a novel drug target for pancreatic cancer.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer death.
  • It has been shown that the growth of PDAC and pancreatic duct epithelial cells is regulated by beta-adrenoreceptors (beta-ARs).
  • The aim of the study was to investigate if GABA B R inhibits beta-AR signaling in PDAC and pancreatic duct epithelial cells, thus blocking driving forces of cancer progression, such as cell proliferation and cell migration.
  • METHODS: Intracellular cAMP was measured by immunoassays, DNA synthesis by BrdU incorporation assays, activation of ERK1/2 by ERK activation assays, and Western blots and metastatic potential by cell migration assays in the human PDAC cell lines PANC-1 and BXPC-3 and immortalized human pancreatic duct epithelial cells HPDE6-C7.
  • DNA synthesis and cell migration were stimulated by isoproterenol, responses blocked by GABA and baclofen.
  • CONCLUSIONS: The data suggest the stimulation of GABA B R signaling as a novel target for the treatment and prevention of pancreatic cancer.

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  • [Copyright] Cancer 2008. (c) 2007 American Cancer Society.
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5272-7 [15958573.001]
  • [Cites] J Cell Biochem. 2005 Jul 1;95(4):649-56 [15849724.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Oct;131(10):639-48 [16091975.001]
  • [Cites] Pancreas. 2005 Nov;31(4):301-16 [16258363.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):369-75 [16428474.001]
  • [Cites] J Clin Anesth. 2005 Dec;17(8):586-91 [16427527.001]
  • [Cites] Int J Cancer. 2006 Mar 15;118(6):1370-80 [16206275.001]
  • [Cites] Invest New Drugs. 2005 Dec;23(6):583-90 [16034525.001]
  • [Cites] Auton Neurosci. 2006 Jan 30;124(1-2):1-8 [16338174.001]
  • [Cites] Int J Cancer. 2006 Jun 1;118(11):2744-9 [16381019.001]
  • [Cites] Biochem Pharmacol. 2006 May 14;71(10):1397-421 [16563357.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Jun;58(3):231-41 [16725343.001]
  • [Cites] Pancreas. 2006 Jul;33(1):53-62 [16804413.001]
  • [Cites] Int J Cancer. 2006 Oct 1;119(7):1547-52 [16671086.001]
  • [Cites] Trends Plant Sci. 2006 Sep;11(9):424-7 [16890474.001]
  • [Cites] J Agric Food Chem. 2006 Sep 6;54(18):6765-75 [16939338.001]
  • [Cites] Plant Physiol. 2006 Dec;142(4):1350-2 [17151138.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):93-8 [17182741.001]
  • [Cites] Toxicol Sci. 2007 Mar;96(1):21-9 [17003101.001]
  • [Cites] Cancer Treat Rev. 2000 Feb;26(1):29-52 [10660490.001]
  • [Cites] Am J Pathol. 2000 Nov;157(5):1623-31 [11073822.001]
  • [Cites] J Cancer Res Clin Oncol. 2000 Nov;126(11):624-30 [11079726.001]
  • [Cites] Carcinogenesis. 2001 Mar;22(3):473-9 [11238189.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2866-9 [11306460.001]
  • [Cites] Oncogene. 2001 Mar 26;20(13):1532-9 [11313899.001]
  • [Cites] Int J Oncol. 2002 Jul;21(1):153-7 [12063562.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):455-63 [12189387.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6467-9 [12438237.001]
  • [Cites] Eur J Pharmacol. 2003 Feb 28;463(1-3):235-72 [12600714.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jul;80(1):63-70 [12889599.001]
  • [Cites] Clin Cancer Res. 2004 May 15;10(10):3327-32 [15161686.001]
  • [Cites] J Biol Chem. 2004 Sep 17;279(38):40209-19 [15210690.001]
  • [Cites] Arch Int Pharmacodyn Ther. 1969 Jun;179(2):343-51 [5367308.001]
  • [Cites] Eur J Cell Biol. 1990 Feb;51(1):76-84 [2328739.001]
  • [Cites] Scand J Clin Lab Invest Suppl. 1990;201:25-43 [1978755.001]
  • [Cites] Eur J Clin Invest. 1992 May;22(5):301-6 [1592082.001]
  • [Cites] Can J Anaesth. 1993 May;40(5 Pt 1):435-9 [8390330.001]
  • [Cites] J Pharmacol Exp Ther. 1996 Jun;277(3):1209-14 [8667180.001]
  • [Cites] Gastroenterology. 1998 Sep;115(3):714-21 [9721169.001]
  • [Cites] Cancer Res. 1999 May 1;59(9):2223-8 [10232612.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4510-5 [10493497.001]
  • [Cites] J Nutr. 2004 Dec;134(12 Suppl):3445S-3452S [15570052.001]
  • [Cites] Biofactors. 2004;22(1-4):165-7 [15630275.001]
  • [Cites] Cesk Fysiol. 2004;53(3):117-24 [15702867.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2005 Jun;29(5):733-7 [15939520.001]
  • (PMID = 18098271.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829; United States / NCI NIH HHS / CA / R01 CA42829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / GABA Agents; 0 / GABA Agonists; 0 / Receptors, GABA; 56-12-2 / gamma-Aminobutyric Acid; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; G34N38R2N1 / Bromodeoxyuridine; H789N3FKE8 / Baclofen; L628TT009W / Isoproterenol
  • [Other-IDs] NLM/ NIHMS381601; NLM/ PMC3375598
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60. Brune K, Abe T, Canto M, O'Malley L, Klein AP, Maitra A, Volkan Adsay N, Fishman EK, Cameron JL, Yeo CJ, Kern SE, Goggins M, Hruban RH: Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer. Am J Surg Pathol; 2006 Sep;30(9):1067-76
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  • [Title] Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer.
  • We screened 116 patients with a strong family history of pancreatic cancer using a combination of endoscopic ultrasound and computed tomography.
  • Ten of these patients underwent surgical resection at our institution, providing an opportunity to define the morphology of pancreatic precursor lesions in patients with a strong family history of pancreatic cancer.
  • The number of pancreatic intraepithelial neoplasia (PanIN) lesions and intraductal papillary mucinous neoplasms (IPMNs) were compared with age-matched controls.
  • PanINs were significantly more common in the 8 cases (mean of 10.7% of the duct profiles, range 1.0% to 27.3%) than in the controls (mean 1.9%, range 0% to 9.2%, P<0.01).
  • Some individuals with a strong family history of pancreatic cancer develop multifocal, noninvasive epithelial precursor lesions of the pancreas.
  • The multifocal nature of familial pancreatic neoplasia suggests that surveillance of these patients is warranted after partial pancreatectomy.

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  • [Cites] Am J Pathol. 1971 Jun;63(3):521-46 [5581235.001]
  • [Cites] Mol Cancer. 2003 Jan 7;2:9 [12556240.001]
  • [Cites] Br J Exp Pathol. 1981 Dec;62(6):547-58 [7326214.001]
  • [Cites] Am J Pathol. 1987 Mar;126(3):439-51 [3826300.001]
  • [Cites] N Engl J Med. 1987 Jun 11;316(24):1511-4 [3587280.001]
  • [Cites] Radiology. 1989 Feb;170(2):411-5 [2536185.001]
  • [Cites] Science. 1991 Aug 9;253(5020):661-5 [1651562.001]
  • [Cites] J Natl Cancer Inst. 1993 Jul 7;85(13):1020-1 [8515481.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1215-25 [8261515.001]
  • [Cites] Endoscopy. 1993 Nov;25(9):555-64 [8119204.001]
  • [Cites] Am J Pathol. 1994 May;144(5):889-95 [8178941.001]
  • [Cites] Gastroenterology. 1996 Mar;110(3):875-84 [8608898.001]
  • [Cites] Semin Oncol. 1996 Apr;23(2):251-75 [8623061.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):7-8 [8782809.001]
  • [Cites] Nature. 1997 Apr 24;386(6627):761, 763 [9126728.001]
  • [Cites] Gastrointest Endosc. 1998 Jul;48(1):11-7 [9684658.001]
  • [Cites] Gastrointest Endosc. 1998 Jul;48(1):18-25 [9684659.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):379-83 [9697701.001]
  • [Cites] Vet Radiol Ultrasound. 1998 Nov-Dec;39(6):557-62 [9845197.001]
  • [Cites] Ann Intern Med. 1999 Aug 17;131(4):247-55 [10454945.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):324-31 [15549094.001]
  • [Cites] Cancer Res. 2005 Mar 1;65(5):1619-26 [15753353.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]
  • [Cites] PLoS Med. 2004 Dec;1(3):e65 [15630470.001]
  • [Cites] Cancer. 2005 Sep 15;104(6):1149-57 [16088887.001]
  • [Cites] Virchows Arch. 2005 Nov;447(5):800-5 [16021508.001]
  • [Cites] Virchows Arch A Pathol Pathol Anat. 1970;349(1):69-79 [4907111.001]
  • [Cites] Am J Pathol. 1975 Aug;80(2):203-26 [169698.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Jun;4(6):766-81; quiz 665 [16682259.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):1208-17 [16424060.001]
  • [Cites] Am J Pathol. 2000 May;156(5):1767-71 [10793087.001]
  • [Cites] Radiol Clin North Am. 2000 Jul;38(4):625-51 [10943268.001]
  • [Cites] Gastroenterology. 2000 Dec;119(6):1447-53 [11113065.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):738-44 [11297271.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] Am J Surg Pathol. 2001 Aug;25(8):1047-53 [11474289.001]
  • [Cites] Cancer J. 2001 Jul-Aug;7(4):266-73 [11561603.001]
  • [Cites] Endoscopy. 2001 Oct;33(10):824-31 [11571676.001]
  • [Cites] Genet Epidemiol. 2002 Aug;23(2):133-49 [12214307.001]
  • [Cites] Gastroenterology. 2002 Oct;123(4):1052-60 [12360467.001]
  • [Cites] Cancer Biol Ther. 2002 Sep-Oct;1(5):571-81 [12496492.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9361-9 [12522141.001]
  • [Cites] Dig Surg. 2003;20(6):520-6 [14534374.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1495-501 [14657708.001]
  • [Cites] J Cell Biochem. 2004 Feb 15;91(3):459-77 [14755677.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2634-8 [15059921.001]
  • [Cites] J Clin Pathol. 2004 May;57(5):456-62 [15113850.001]
  • [Cites] Clin Gastroenterol Hepatol. 2004 Jul;2(7):606-21 [15224285.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):977-87 [15252303.001]
  • [CommentIn] Am J Surg Pathol. 2007 Apr;31(4):645-6 [17414117.001]
  • (PMID = 16931950.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA062924-140011; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA062924-120011; United States / NCI NIH HHS / CA / P50 CA062924-130011; United States / NCI NIH HHS / CA / P50 CA062924-120011; United States / NCI NIH HHS / CA / R01 CA97075; United States / NCI NIH HHS / CA / R01 CA097075; United States / NCI NIH HHS / CA / CA062924-130011; United States / NCI NIH HHS / CA / CA062924-140011
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS105552; NLM/ PMC2746409
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61. Hsu HP, Shan YS, Lai MD, Lin PW: Osteopontin-positive infiltrating tumor-associated macrophages in bulky ampullary cancer predict survival. Cancer Biol Ther; 2010 Jul 15;10(2):144-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osteopontin-positive infiltrating tumor-associated macrophages in bulky ampullary cancer predict survival.
  • PURPOSE: Tumor-associated macrophages (TAMs) promote cancer cell proliferation and distant metastases.
  • Osteopontin (OPN) is overexpressed in several human cancer cells and in TAMs.
  • Therefore, we set out to determine the role of OPN-expressing macrophages in cancer.
  • Expression patterns of OPN in TAMs were associated with pancreatic invasion, tumor stage, TNM stage, lymphovascular invasion and recurrence with peritoneal carcinomatosis.
  • Macrophage-associated cytokine expression in ampullary cancer cells was also assessed; levels of macrophage migration inhibitory factor (MIF) in cancer cells were higher than in normal duodenal mucosa.
  • EXPERIMENTAL DESIGN: Specimens from ampullary cancer patients at National Cheng Kung University Hospital were collected for immunohistochemistry.
  • CONCLUSIONS: Expression of OPN and location of TAMs in bulky ampullary cancer predict recurrence.
  • In addition, cytoplasmic staining of MIF is enhanced in ampullary cancer cells.
  • [MeSH-major] Adenocarcinoma / pathology. Ampulla of Vater / pathology. Biomarkers, Tumor / metabolism. Common Bile Duct Neoplasms / pathology. Macrophage Migration-Inhibitory Factors / metabolism. Macrophages / metabolism. Osteopontin / metabolism. RNA, Neoplasm / metabolism

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  • (PMID = 20495367.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Macrophage Migration-Inhibitory Factors; 0 / RNA, Neoplasm; 106441-73-0 / Osteopontin
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62. Zhang L, Notohara K, Levy MJ, Chari ST, Smyrk TC: IgG4-positive plasma cell infiltration in the diagnosis of autoimmune pancreatitis. Mod Pathol; 2007 Jan;20(1):23-8
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  • [Title] IgG4-positive plasma cell infiltration in the diagnosis of autoimmune pancreatitis.
  • Autoimmune pancreatitis typically produces an enlarged pancreas with narrowing of the pancreatic duct, and can mimic carcinoma.
  • Autoimmune pancreatitis usually responds to corticosteroid treatment, making it important to differentiate from pancreatic ductal adenocarcinoma.
  • We investigated the role of IgG4 staining in the diagnosis of autoimmune pancreatitis, first in resected pancreas specimens (29 autoimmune pancreatitis, nine chronic alcoholic pancreatitis and 25 pancreatic cancer), then in pancreatic needle biopsies.
  • When we subdivided autoimmune pancreatitis into the histologic subtypes lymphoplasmacytic sclerosing pancreatitis and idiopathic duct-destructive pancreatitis, 16/17 lymphoplasmacytic sclerosing pancreatitis had moderate to marked staining, compared to five to 12 idiopathic duct-destructive pancreatitis.
  • We conclude that pancreatic tissue from patients with autoimmune pancreatitis often shows moderate or marked infiltration by IgG4-positive plasma cells (>10/HPF).
  • We rarely see IgG4 staining in patients with chronic alcoholic pancreatitis and pancreatic ductal adenocarcinoma.
  • [MeSH-minor] Adenocarcinoma / immunology. Adenocarcinoma / pathology. Adolescent. Aged. Biomarkers / analysis. Carcinoma, Pancreatic Ductal / immunology. Carcinoma, Pancreatic Ductal / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Pancreatic Neoplasms / immunology. Pancreatic Neoplasms / pathology. Pancreatitis, Alcoholic / immunology. Pancreatitis, Alcoholic / pathology. Severity of Illness Index

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  • (PMID = 16980948.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Immunoglobulin G
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63. Chu PG, Schwarz RE, Lau SK, Yen Y, Weiss LM: Immunohistochemical staining in the diagnosis of pancreatobiliary and ampulla of Vater adenocarcinoma: application of CDX2, CK17, MUC1, and MUC2. Am J Surg Pathol; 2005 Mar;29(3):359-67
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  • [Title] Immunohistochemical staining in the diagnosis of pancreatobiliary and ampulla of Vater adenocarcinoma: application of CDX2, CK17, MUC1, and MUC2.
  • We studied the expression of cytokeratin 7 (CK7), cytokeratin 17 (CK17), cytokeratin 20 (CK20), CDX2, mucin 1 (MUC1), mucin 2 (MUC2), and mucin 5AC (MUC5AC) in 46 cases of pancreatic ductal carcinoma, 18 ampulla of Vater adenocarcinomas, and 24 intrahepatic cholangiocarcinomas.
  • The expression of MUC1 and CK17 was restricted to pancreatic ductal carcinoma (41 of 46, 89%; 38 of 46, 83%, respectively), the ampullary carcinoma of pancreatobiliary origin (6 of 6, 100%; 5 of 6, 83%, respectively), and intrahepatic cholangiocarcinoma (20 of 24, 83%; 17 of 24, 71%, respectively).
  • The expression of MUC2 and CDX2 was restricted to the intestinal, mucinous, and signet-ring cell-type adenocarcinomas of duodenal papillary origin (9 of 11, 82%; 11 of 11, 100%, respectively).
  • MUC2 was rarely expressed in pancreatic ductal carcinoma (1 of 46, 2%) and was negative in the ampullary carcinoma of pancreatobiliary origin and in intrahepatic cholangiocarcinoma.
  • A heterogeneous CDX2 staining pattern was seen in 1 of 6 cases of the ampullary carcinoma of pancreatobiliary origin (17%), 5 of 24 intrahepatic cholangiocarcinomas (21%), and 10 of 46 (22%) pancreatic ductal carcinomas.
  • In contrast, all 11 cases of the intestinal, mucinous, and signet-ring cell-type adenocarcinomas of duodenal papillary origin showed homogeneous CDX2 nuclear positivity.
  • MUC1+/CK17+ can be used as positive markers for pancreatic ductal carcinomas, the ampullary carcinoma of pancreatobiliary origin, and cholangiocarcinomas with positive predictive values of 76%, 83%, and 58%, respectively.
  • MUC2+/CDX2+ can be used as positive markers for the intestinal-type adenocarcinoma of duodenal papillary origin with a positive predictive value of 82%.
  • [MeSH-major] Ampulla of Vater / pathology. Bile Ducts, Intrahepatic / pathology. Carcinoma, Pancreatic Ductal / pathology. Cholangiocarcinoma / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratins / metabolism. Male. Mucins / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 15725805.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Mucins; 0 / Neoplasm Proteins; 68238-35-7 / Keratins
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64. Kelly KA, Bardeesy N, Anbazhagan R, Gurumurthy S, Berger J, Alencar H, Depinho RA, Mahmood U, Weissleder R: Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma. PLoS Med; 2008 Apr 15;5(4):e85
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  • [Title] Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, typically presenting with metastasis at the time of diagnosis and exhibiting profound resistance to existing therapies.
  • METHODS AND FINDINGS: Here, a phage display approach was used in a mouse model of PDAC to screen for peptides that specifically bind to cell surface antigens on PDAC cells.
  • These screens yielded a motif that distinguishes PDAC cells from normal pancreatic duct cells in vitro, which, upon proteomics analysis, identified plectin-1 as a novel biomarker of PDAC.

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  • [Cites] Cancer Cell. 2003 Nov;4(5):393-403 [14667506.001]
  • [Cites] Mol Biol Cell. 2007 Nov;18(11):4210-21 [17699601.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Lancet. 2004 Mar 27;363(9414):1049-57 [15051286.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18701-10 [14966116.001]
  • [Cites] Clin Gastroenterol Hepatol. 2004 Jul;2(7):606-21 [15224285.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):250-60 [15236190.001]
  • [Cites] Bioconjug Chem. 2004 Sep-Oct;15(5):1062-7 [15366960.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2643-9 [8168092.001]
  • [Cites] Anal Chem. 1995 Apr 15;67(8):1426-36 [7741214.001]
  • [Cites] Ann Surg. 1995 Oct;222(4):580-8; discussion 588-92 [7574936.001]
  • [Cites] J Magn Reson Imaging. 1997 Jan-Feb;7(1):258-63 [9039625.001]
  • [Cites] Nat Biotechnol. 1997 Nov;15(12):1271-5 [9359110.001]
  • [Cites] Genes Dev. 1998 Nov 1;12(21):3442-51 [9808630.001]
  • [Cites] J Leukoc Biol. 2002 May;71(5):821-8 [11994507.001]
  • [Cites] Acad Radiol. 2002 Aug;9 Suppl 2:S304-6 [12188255.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2003;4:237-56 [14527303.001]
  • [Cites] Ann Intern Med. 1999 Aug 17;131(4):247-55 [10454945.001]
  • [Cites] J Invest Dermatol. 1999 Sep;113(3):422-3 [10469345.001]
  • [Cites] J Natl Cancer Inst. 2004 Nov 3;96(21):1571 [15523083.001]
  • [Cites] Circ Res. 2005 Feb 18;96(3):327-36 [15653572.001]
  • [Cites] Methods Mol Med. 2005;103:175-87 [15542906.001]
  • [Cites] J Clin Oncol. 2005 Jul 10;23(20):4524-31 [16002843.001]
  • [Cites] Bioconjug Chem. 2005 Sep-Oct;16(5):1240-5 [16173804.001]
  • [Cites] Int J Cancer. 2005 Nov 10;117(3):335-9 [15900588.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2592-9 [16510577.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5947-52 [16585505.001]
  • [Cites] J Cell Sci. 2006 May 1;119(Pt 9):1864-75 [16608880.001]
  • [Cites] Mol Imaging. 2006 Jan-Mar;5(1):24-30 [16779967.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1269-81 [16814714.001]
  • [Cites] Bioconjug Chem. 2006 Jul-Aug;17(4):905-11 [16848396.001]
  • [Cites] Neoplasia. 2006 Sep;8(9):772-80 [16984734.001]
  • [Cites] Neoplasia. 2006 Dec;8(12):1011-8 [17217618.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):211-3 [17349578.001]
  • [Cites] Exp Cell Res. 2007 Jun 10;313(10):2189-203 [17499243.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Semin Oncol. 2007 Aug;34(4):284-94 [17674956.001]
  • [Cites] Am J Gastroenterol. 2007 Oct;102(10):2157-63 [17897335.001]
  • [Cites] Neoplasia. 2003 Sep-Oct;5(5):437-44 [14670181.001]
  • (PMID = 18416599.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA086355; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / K01 CA104647-03; United States / NCI NIH HHS / CA / P50-CA86355; United States / NCI NIH HHS / CA / P01-CA117969-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides; 0 / Plec protein, mouse; 0 / Plectin
  • [Other-IDs] NLM/ PMC2292750
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65. Corbo V, Ritelli R, Barbi S, Funel N, Campani D, Bardelli A, Scarpa A: Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas. PLoS One; 2010;5(9):e12653
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  • [Title] Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas.
  • Tumours of the pancreas are aggressive neoplasms for which no effective therapeutic strategy is currently available.
  • METHODOLOGY/PRINCIPAL FINDINGS: We conducted a DNA-sequence analysis of a selected set of 35 kinase genes in a panel of 52 pancreatic exocrine neoplasms, including 36 pancreatic ductal adenocarcinoma, and 16 ampulla of Vater cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Common Bile Duct Neoplasms / genetics. Mutation. Pancreatic Neoplasms / genetics. Protein Kinases / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Ampulla of Vater / enzymology. Base Sequence. Cell Line, Tumor. Female. Humans. Male. Middle Aged. Molecular Sequence Data